Wednesday, 31 July 2013
Tuesday, 30 July 2013
Guava Leaves "Serious Medicine for Modern Health Challenges"
The young leaves of the guava plant are used in traditional medicine in tropical countries. These leaves contain a number of beneficial substances, including antioxidants like vitamin C and flavonoids such as quercetin. Drinking a tea made by soaking guava leaves in hot water may be beneficial in treating diarrhea, lowering cholesterol and preventing diabetes.
Guava leaf tea may help to inhibit a variety of diarrhea-causing bacteria. People with diarrhea who drink this type of tea may experience fewer stools, less abdominal pain, less watery stools and a quicker recovery, according to Drugs.com. A study published in the "Revista do Instituto de Medicina Tropical de São Paulo" in 2008 found that guava-leaf extracts inhibited the growth of Staphylococcus aureus bacteria, which is a common cause of diarrhea.
Drinking guava leaf tea may cause beneficial changes in your cholesterol and triglyceride levels. Study participants who drank guava leaf tea had lower total cholesterol, low-density lipoprotein levels and triglycerides after eight weeks whether or not they were receiving medical treatment to lower their cholesterol levels, according to an article published in "Nutrition & Metabolism" in February 2010. Their levels of beneficial high-density lipoprotein were not affected. Other trials have shown similar benefits, with study lengths ranging from four weeks to 12 weeks and doses ranging from 0.4 to 1 kilogram per day, according to Drugs.com.
Diarrhea
Guava leaf tea may help to inhibit a variety of diarrhea-causing bacteria. People with diarrhea who drink this type of tea may experience fewer stools, less abdominal pain, less watery stools and a quicker recovery, according to Drugs.com. A study published in the "Revista do Instituto de Medicina Tropical de São Paulo" in 2008 found that guava-leaf extracts inhibited the growth of Staphylococcus aureus bacteria, which is a common cause of diarrhea.
High Cholesterol
Drinking guava leaf tea may cause beneficial changes in your cholesterol and triglyceride levels. Study participants who drank guava leaf tea had lower total cholesterol, low-density lipoprotein levels and triglycerides after eight weeks whether or not they were receiving medical treatment to lower their cholesterol levels, according to an article published in "Nutrition & Metabolism" in February 2010. Their levels of beneficial high-density lipoprotein were not affected. Other trials have shown similar benefits, with study lengths ranging from four weeks to 12 weeks and doses ranging from 0.4 to 1 kilogram per day, according to Drugs.com.
Diabetes
Japan has approved guava leaf tea as one of the Foods for Specified Health Uses to help with the prevention and treatment of diabetes. Compounds in the tea inhibit the absorption of two types of sugars, maltose and sucrose, helping to control blood sugar levels after meals. The article published in "Nutrition & Metabolism" described two studies showing this effect. The first study showed the short-term benefits, as participants who drank guava leaf tea after consuming white rice had decreases in blood sugar that were greater after 30 minutes, 90 minutes and 120 minutes than when the same study participants ate the same amount of white rice followed by drinking hot water. In the second, longer-term study participants with either prediabetes or mild Type 2 diabetes who drank guava leaf tea with every meal for 12 weeks had lower fasting blood-sugar levels than before they started drinking the tea.
http://www.guavaleafextract.com/
http://www.specialtyproduce.com/produce/Guava_Leaves_8500.php
http://health.excite.co.uk/guava-leaves.html
Monday, 29 July 2013
Smoking Health Risks
Why quit smoking?
Most people know that smoking can cause lung cancer, but it can also cause many other cancers and illnesses. Smoking directly causes over 100,000 deaths in the UK each year and contributes to many more.
Of these deaths, about 42,800 are from smoking-related cancers, 30,600 from cardiovascular disease and 29,100 die slowly from emphysema and other chronic lung diseases.
How do cigarettes damage health?
Cigarettes contain more than 4000 chemical compounds and at least 400 toxic substances.
When you inhale, a cigarette burns at 700°C at the tip and around 60°C in the core. This heat breaks down the tobacco to produce various toxins. As a cigarette burns, the residues are concentrated towards the butt.
The products that are most damaging are:
tar, a carcinogen (substance that causes cancer)
nicotine is addictive and increases cholesterol levels in your body
carbon monoxide reduces oxygen in the body
components of the gas and particulate phases cause chronic obstructive pulmonary disorder (COPD).
The damage caused by smoking is influenced by:
the number of cigarettes smoked
whether the cigarette has a filter
how the tobacco has been prepared.
The products that are most damaging are:
tar, a carcinogen (substance that causes cancer)
nicotine is addictive and increases cholesterol levels in your body
carbon monoxide reduces oxygen in the body
components of the gas and particulate phases cause chronic obstructive pulmonary disorder (COPD).
The damage caused by smoking is influenced by:
the number of cigarettes smoked
whether the cigarette has a filter
how the tobacco has been prepared.
Smoking affects how long you live
Research has shown that smoking reduces life expectancy by seven to eight years.
Of the 300 people who die every day in the UK as a result of smoking, many are comparatively young smokers.
The number of people under the age of 70 who die from smoking-related diseases exceeds the total figure for deaths caused by breast cancer, AIDS, traffic accidents and drug addiction.
The number of people under the age of 70 who die from smoking-related diseases exceeds the total figure for deaths caused by breast cancer, AIDS, traffic accidents and drug addiction.
Non-smokers and ex-smokers can also look forward to a healthier old age than smokers.
http://en.wikipedia.org/wiki/Health_effects_of_tobacco
http://www.netdoctor.co.uk/health_advice/facts/smokehealth.htm#ixzz2aSXZcC2Z
http://www.tobaccofreemaine.org/channels/parents/learn_more_about_health_effects.php
Sunday, 28 July 2013
Saturday, 27 July 2013
Immunology III. ADAPTIVE IMMUNE RESPONSE
FUNCTIONAL BRANCHES OF THE ADAPTIVE IMMUNE RESPONSE:
- T-CELL–MEDIATED IMMUNE RESPONSES (CELL-MEDIATED IMMUNITY)
- HUMORAL IMMUNITY
T-CELL–MEDIATED IMMUNE RESPONSES (CELL-MEDIATED IMMUNITY)
A. T-cell activation. Upon activation by antigen, signals from the TCR and coreceptors alter the pattern of gene transcription for proliferation and differentiation into effector T cells (TH1, TH2, or CTL). The effector activity of the T cell is accomplished through the cytokines that the T cell produces (see Table: MAJOR PROPERTIES OF SELECTED CYTOKINES). TCR binding to antigen and initial T-cell activation involves a cascade of signaling events that include the transcription factors NF kB, nuclear factor of activated T cells (NFAT), and activator protein 1 (AP-1). The production of IL-2 in response to T-cell activation is important for the initial proliferation and differentiation of the T cell. The immunosuppressive drugs cyclosporine A and tacrolimus (also called FK506) disrupt the signals from the TCR, thereby inhibiting the production of IL-2. Rapamycin inhibits the signaling from the IL-2 receptor.
B. T-cell effector functions
1. Nonviral intracellular parasites such as mycobacteria, Listeria, and certain protozoa are primarily eliminated by T-cell–macrophage immunity. Antigen-specific TH1 cell activation with the release of IFN-g and other macrophage-activating factors enhances effective immunity to these bacterial intracellular pathogens.
1. Nonviral intracellular parasites such as mycobacteria, Listeria, and certain protozoa are primarily eliminated by T-cell–macrophage immunity. Antigen-specific TH1 cell activation with the release of IFN-g and other macrophage-activating factors enhances effective immunity to these bacterial intracellular pathogens.
2. Viruses must be eliminated from both extracellular sites and infected cells.
a. Antibodies neutralize virus particles in blood and tissue fluids to prevent further infection of host cells. These antibodies also serve as opsonins to assist with phagocytosis. Antibodies are generally ineffective against infected cells.
b. CTL cells recognize infected cells via class I MHC presentation of viral peptides. The CTL then directly kills the infected cells in an antigen-specific manner and secretes lymphokines, such as IFN-g. Cytotoxic granule release (granulolysin, perforin, and granzymes) by the CTL is focused toward the infected cell, which is triggered to die by apoptosis; healthy, nearby cells are not affected. In addition, CTLs can induce apoptosis via FAS ligand binding to FAS on the target cells.
c. NK cells kill infected (and tumor) cells in a non–antigen-specific manner by binding to MHClike molecules using a variety of receptors. NK cells kill their target cells using mechanisms similar to those used by CTLs.
d. IFN-g (secreted by CTL, NK, and TH1 cells) and IFN-a and IFN-b (secreted by fibroblasts and other cells) provide additional antiviral immunity by binding to receptors on nearby uninfected cells to induce the synthesis of kinases and endonucleases (i.e., antiviral proteins), which inhibit viral and cellular growth. Interferons also upregulate MHC protein expression, which makes infected cells more visible to T cells.
3. Tumors are modified host cells and must be eliminated by the immune system, usually by cell mediated immunity via CTL and NK cells.
4. Graft rejection (will be discussed later)
C. T-cell memory. T-cell immune responses give rise to long-lived immunological memory (memory cells) and protective immunity.
HUMORAL IMMUNITY
A. Overview. The production of antibodies is the major focus of the B-cell portion of the immune system. The function of an antibody is to recognize and bind to its corresponding foreign antigen in order to prevent that antigen from functioning (neutralization) or to target the antigen to other components of the immune system. Most antibody responses involve the activation of both B and TH cells. T-independent responses to certain antigens do not require TH cells. These antigens tend to either interact with other PRRs (e.g., bacterial LPS) or are highly repetitive antigens (e.g., bacterial cell wall carbohydrates). T-cell–independent responses generally produce only IgM and do not produce a memory B-cell response.
B. Primary immune response. The first time a specific antigen is encountered, only naive B cells and naive TH cells are present to respond to the antigen. In the secondary lymph tissue, B cells and T cells are closely associated with each other such that proliferation and differentiation of antigen specific B and T cells can occur simultaneously. Germinal centers develop in secondary lymph tissue as a result of the lymphocyte proliferation during an immune response. Activated lymphocytes differentiate into short-lived effector cells and long-lived memory cells. Some of the activated B cells differentiate into plasma cells secreting IgM of low affinity. Later in the immune response, under the direction of the TH cells, B cells will undergo isotype switching such that plasma cells producing other classes of antibody will develop. The primary humoral immune response is detected in the serum after 4 days and peaks at 7 to 14 days.
C. Affinity maturation. Under the influence of TH cells, B cells undergo somatic hypermutation, which introduces point mutations into the immunoglobulin genes such that the expanding population of B cells will produce BCRs with altered antigen-binding sites. Only those B cells that have produced immunoglobulins with a greater affinity for the antigens, as demonstrated by the ability to interact with antigen present in the lymph tissue, will be allowed to mature. In this way, the antibody response matures to produce antibodies with increasing binding affinity.
D. Isotype switching. After B-cell activation, TH cells secrete cytokines to direct isotype switching to produce different classes (isotypes) of antibody. Antigen binding is unaffected by the isotype change. TH2 cytokines, chiefly IL-4, IL-5, and TGF-b, lead to the production of IgA and IgE, as well as weakly opsonizing antibody, such as IgG2 and IgG4. TH1 cells direct the production of opsonizing antibodies, chiefly IgG1 (see Table: MAJOR PROPERTIES OF SELECTED CYTOKINES).
E. Memory immune responses. The creation of memory B and T cells establishes immunological memory. Long-lived memory B cells retain surface immunoglobulin with the selected antigen affinity and of the selected isotype, in the event the same antigen is encountered again. Memory cells more rapidly respond to the presence of the antigen (2 to 3 days after reencountering the antigen), and the absolute amount of specific antibody is greater. For some immune responses, but not all, memory is lifelong.
F. Immunoglobulins: Antigen binding and class-specific functions. In this chapter, the terms antibody and immunoglobulin are used interchangeably.
1. Structure.
The mechanism for generating diversity in the variable portion of the H and L chains is based on the requirement for gene rearrangement of the antibody gene segments during lymphocyte development. The germ line H and L chain genes are nonfunctional until gene segments are rearranged during B-cell development to create a functional gene. The number of different immunoglobulin gene segments, coupled with junctional and insertional variability during DNA recombination, accounts for an enormous number of different potential immunoglobulin sequences, and thus antigen binding for antibodies.
2. Class. There are five general heavy-chain, constant-region amino acid sequences. These determine the five general classes of immunoglobulins: IgM, IgG, IgE, IgA, and IgD. Within some classes, variants of heavy-chain amino acid sequence yield subclasses: IgG1–4 and IgA1–2. The class of an immunoglobulin defines the transport of the antibody throughout the body, as well as the ability of the antibody to interact with other components of the immune system.
a. IgM is the first antibody produced in response to a new infection. The IgM is present on the surface of the mature naive B cells as a monomer, whereas IgM is secreted from the plasma cell as a pentamer. As the first antibody produced, IgM tends to have low binding affinity; however, it is able to bind strongly because it has 10 antigen-binding sites. IgM is present in the blood and tissues, although it does not penetrate tissues well because of its large size. IgM is the most potent activator of the complement system via the classical pathway. Its serum half-life is 9 to 11 days.
b. IgD is produced on the surface of mature naive B cells simultaneously with IgM and serves as a marker for maturation. It is present in very small amounts in the serum and does not appear to be produced as a secreted antibody by plasma cells.
c. IgG is the predominant serum immunoglobulin secreted at the end of the primary immune responses and during memory responses. There are four subclasses of IgG in humans, each with differences in function. IgG has the longest lasting serum half-life (21 days for most subclasses) and is the most plentiful antibody in the serum. IgG (especially IgG3) is able to activate complement via the classical pathway. IgG1, IgG2, and IgG3 are opsonic and enhance the phagocyte’s ability to engulf the pathogen when it is coated in IgG. The FcRn receptor transports IgG across endothelial cells into the tissues and can also selectively transport IgG across the placenta into the fetus during the last trimester of pregnancy.
d. IgA can be expressed as either a monomer (in the blood and tissues) or a dimer (at mucosal surfaces). Dimeric IgA is secreted in large quantities across mucosal surfaces into gastrointestinal, respiratory, lachrymal, mammary, and genitourinary secretions, where it protects the mucosa from colonization.
e. IgE is the least plentiful antibody in the serum. IgE is made in small quantities and is rapidly bound irreversibly to the high affinity FceRI receptors present on mast cells, basophils, and eosinophils. Antigen binding to the IgE on the surface of the mast cell signals activation and degranulation of the mast cell.
a. IgM is the first antibody produced in response to a new infection. The IgM is present on the surface of the mature naive B cells as a monomer, whereas IgM is secreted from the plasma cell as a pentamer. As the first antibody produced, IgM tends to have low binding affinity; however, it is able to bind strongly because it has 10 antigen-binding sites. IgM is present in the blood and tissues, although it does not penetrate tissues well because of its large size. IgM is the most potent activator of the complement system via the classical pathway. Its serum half-life is 9 to 11 days.
b. IgD is produced on the surface of mature naive B cells simultaneously with IgM and serves as a marker for maturation. It is present in very small amounts in the serum and does not appear to be produced as a secreted antibody by plasma cells.
c. IgG is the predominant serum immunoglobulin secreted at the end of the primary immune responses and during memory responses. There are four subclasses of IgG in humans, each with differences in function. IgG has the longest lasting serum half-life (21 days for most subclasses) and is the most plentiful antibody in the serum. IgG (especially IgG3) is able to activate complement via the classical pathway. IgG1, IgG2, and IgG3 are opsonic and enhance the phagocyte’s ability to engulf the pathogen when it is coated in IgG. The FcRn receptor transports IgG across endothelial cells into the tissues and can also selectively transport IgG across the placenta into the fetus during the last trimester of pregnancy.
d. IgA can be expressed as either a monomer (in the blood and tissues) or a dimer (at mucosal surfaces). Dimeric IgA is secreted in large quantities across mucosal surfaces into gastrointestinal, respiratory, lachrymal, mammary, and genitourinary secretions, where it protects the mucosa from colonization.
e. IgE is the least plentiful antibody in the serum. IgE is made in small quantities and is rapidly bound irreversibly to the high affinity FceRI receptors present on mast cells, basophils, and eosinophils. Antigen binding to the IgE on the surface of the mast cell signals activation and degranulation of the mast cell.
3. Specificity. The specificity of each immunoglobulin for antigen binding resides in the two identical antigen-binding sites, each formed by the combination of the variable regions of heavy and light chains.
4. Quantitation of immunoglobulin: Antigen binding and cross-reactivity. Between 108 and 1011, unique immunoglobulins with different antigen-binding specificities are formed by the immune system. B cells are constantly being replaced at a rate of about 2.5 billion per day in a healthy, young adult by production in the bone marrow.
a. Cross-reactive antibodies are those that are able to bind to different, but closely structurally related, antigens. Cross-reactivity may also occur through the sharing of some, but not all, antigens by two strains of bacteria, viruses, or other microorganisms.
b. Each antigen has the potential to activate multiple B cells, and microorganisms have several antigens; therefore, each immune response will elicit the production of multiple antibodies with unique specificities. This response is known as a polyclonal response.
Comprehensive Pharmacy Review
Wikipedia
http://www.uic.edu/classes/bios/bios100/lectures/immune.htm
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108501/
Some pictures in this article are found by google search;
http://textbookofbacteriology.net/imgcid.jpg
http://www.uic.edu/classes/bios/bios100/lectures/1100361_015.jpg
http://www.uic.edu/classes/bios/bios100/lectures/49_14_T_cell_activation-L.jpg
http://www.biolegend.com/pop_pathway.php?id=13
http://visualscience.ru/feature-img/immunoglobulin/igg-zoom2.jpg
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Friday, 26 July 2013
Thursday, 25 July 2013
Your Brain on Drugs: Alcohol
How alcohol molecules alter your brain, ultimately resulting in a night that you...hopefully remember.
Wednesday, 24 July 2013
3 Health Benefits to Drinking Black Tea
The health benefits of black tea have been well documented for quite some time, and if you are thinking of adding more black tea to your diet, then its health benefits likely have played a big part in your decision.
1. Very Low in Sodium, Fat and Calories
Provided that you drink black tea that is pure and plain, and without
the addition of sweeteners, you are drinking a tea that is ultra low in
sodium, fat and calories. This property of black tea is advantageous for
people who want to lose weight or even just control their weight. In
essence, if you merely substitute the intake of other kinds of beverages
like unhealthy soda drinks with black tea, you are already doing your
body a great favor in sparing it the intake of weight gain
causing calories. Furthermore, if you drink more black tea in place of
other beverages that contain higher amounts of sodium and fat, you are
helping your body become more healthy. Too much sodium is linked with
all kinds of lethal conditions and diseases, while too much fat amounts
to the same thing.
2. Reduce Cardiovascular Problems
Certain studies over the years have established that there is a direct
relationship between increased black tea consumption and a decrease in
cardiovascular disease. In 2001, Boston University found in a study that
both short-term as well as long-term drinking of black tea actually
reverses something called endothelial vasomotor dysfunction in patients
with coronary artery disease.
This is a dysfunction which basically serves as a predictor for even
more serious coronary events. The conclusions in the study backed up a
previously held link between black tea and its propensity to lower
cardiovascular problems.
3. Bountiful in Antioxidants
Another benefit of drinking black tea is a sizable one: the abundance of antioxidants in it. Black tea is made from the camellia tea plant. The great benefit of this tea plant is that it comes with a plethora of the group of chemical substances known as poly phenol. These substances are one type of antioxidant, and antioxidants have been found to help in everything from the treatment of brain injury cases to treatments against hearing loss and also, potentially, Parkinson's disease. They are, however, no longer thought to significantly help fight diseases like cancer as they once were thought to.
http://en.wikipedia.org/wiki/Black_tea
http://www.webmd.com/vitamins-supplements/ingredientmono-997-BLACK%20TEA.aspx?activeIngredientId=997&activeIngredientName=BLACK%20TEA
http://www.fitday.com/fitness-articles/nutrition/healthy-eating/3-health-benefits-to-drinking-black-tea.html
Amazing Heart Facts
The heart is the body's engine room, responsible for pumping life-sustaining blood via a 60,000-mile-long (97,000-kilometer-long) network of vessels. The organ works ceaselessly, beating 100,000 times a day, 40 million times a year—in total clocking up three billion heartbeats over an average lifetime. It keeps the body freshly supplied with oxygen and nutrients, while clearing away harmful waste matter.
The fetal heart evolves through several different stages inside the womb, first resembling a fish's heart, then a frog's, which has two chambers, then a snake's, with three, before finally adopting the four-chambered structure of the human heart.
About the size of its owner's clenched fist, the organ sits in the middle of the chest, behind the breastbone and between the lungs, in a moistened chamber that is protected all round by the rib cage. It's made up of a special kind of muscle (cardiac muscle) that works involuntarily, so we don't have to think about it. The heart speeds up or slow downs automatically in response to nerve signals from the brain that tell it how much the body is being exerted. Normally the heart contracts and relaxes between 70 and 80 times per minute, each heartbeat filling the four chambers inside with a fresh round of blood.
These cavities form two separate pumps on each side of the heart, which are divided by a wall of muscle called the septum. The upper chamber on each side is called the atrium. This is connected via a sealing valve to the larger, more powerful lower chamber, or ventricle. The left ventricle pumps most forcefully, which is why a person's heartbeat is felt more on the left side of the chest.
When the heart contracts, the chambers become smaller, forcing blood first out of the atria into the ventricles, then from each ventricle into a large blood vessel connected to the top of the heart. These vessels are the two main arteries. One of them, the pulmonary artery, takes blood to the lungs to receive oxygen. The other, the aorta, transports freshly oxygenated blood to the rest of the body. The vessels that bring blood to the heart are the veins. The two main veins that connect to the heart are called the vena cava.
Since the heart lies at the center of the blood delivery system, it is also central to life. Blood both supplies oxygen from the lungs to the other organs and tissues and removes carbon dioxide to the lungs, where the gas is breathed out. Blood also distributes nourishment from the digestive system and hormones from glands. Likewise our immune system cells travel in the bloodstream, seeking out infection, and blood takes the body's waste products to the kidneys and liver to be sorted out and trashed.
Given the heart's many essential functions, it seems wise to take care of it. Yet heart disease has risen steadily over the last century, especially in industrialized countries, due largely to changes in diet and lifestyle. It has become the leading cause of death for both men and women in the United States, claiming almost 700,000 lives a year, or 29 percent of the annual total. Worldwide, 7.2 million people die from heart disease every year.
The fetal heart evolves through several different stages inside the womb, first resembling a fish's heart, then a frog's, which has two chambers, then a snake's, with three, before finally adopting the four-chambered structure of the human heart.
About the size of its owner's clenched fist, the organ sits in the middle of the chest, behind the breastbone and between the lungs, in a moistened chamber that is protected all round by the rib cage. It's made up of a special kind of muscle (cardiac muscle) that works involuntarily, so we don't have to think about it. The heart speeds up or slow downs automatically in response to nerve signals from the brain that tell it how much the body is being exerted. Normally the heart contracts and relaxes between 70 and 80 times per minute, each heartbeat filling the four chambers inside with a fresh round of blood.
These cavities form two separate pumps on each side of the heart, which are divided by a wall of muscle called the septum. The upper chamber on each side is called the atrium. This is connected via a sealing valve to the larger, more powerful lower chamber, or ventricle. The left ventricle pumps most forcefully, which is why a person's heartbeat is felt more on the left side of the chest.
When the heart contracts, the chambers become smaller, forcing blood first out of the atria into the ventricles, then from each ventricle into a large blood vessel connected to the top of the heart. These vessels are the two main arteries. One of them, the pulmonary artery, takes blood to the lungs to receive oxygen. The other, the aorta, transports freshly oxygenated blood to the rest of the body. The vessels that bring blood to the heart are the veins. The two main veins that connect to the heart are called the vena cava.
Blood Delivery
Since the heart lies at the center of the blood delivery system, it is also central to life. Blood both supplies oxygen from the lungs to the other organs and tissues and removes carbon dioxide to the lungs, where the gas is breathed out. Blood also distributes nourishment from the digestive system and hormones from glands. Likewise our immune system cells travel in the bloodstream, seeking out infection, and blood takes the body's waste products to the kidneys and liver to be sorted out and trashed.
Given the heart's many essential functions, it seems wise to take care of it. Yet heart disease has risen steadily over the last century, especially in industrialized countries, due largely to changes in diet and lifestyle. It has become the leading cause of death for both men and women in the United States, claiming almost 700,000 lives a year, or 29 percent of the annual total. Worldwide, 7.2 million people die from heart disease every year.
http://science.nationalgeographic.com/science/health-and-human-body/human-body/heart-article/
http://www.livescience.com/11351-top-10-amazing-facts-heart.html
http://www.pbs.org/wgbh/nova/heart/heartfacts.html
Tuesday, 23 July 2013
The Miracle of Green Tea
What makes green tea so special?
The secret of green tea lies in the fact it is rich in catechin polyphenols, particularly epigallocatechin gallate (EGCG). EGCG is a powerful anti-oxidant: besides inhibiting the growth of cancer cells, it kills cancer cells without harming healthy tissue. It has also been effective in lowering LDL cholesterol levels, and inhibiting the abnormal formation of blood clots. The latter takes on added importance when you consider that thrombosis (the formation of abnormal blood clots) is the leading cause of heart attacks and stroke.
Harmful Effects?
To date, the only negative side effect reported from drinking green tea is insomnia due to the fact that it contains caffeine. However, green tea contains less caffeine than coffee: there are approximately thirty to sixty mg. of caffeine in six - eight ounces of tea, compared to over one-hundred mg. in eight ounces of coffee.
How to Brew a Cup of Green Tea ?
Producing the perfect cup of green tea is a tricky process. If not handled properly,
those same polyphenols that provide health benefits can ruin the flavor, making the tea
taste "grassy." It's particularly important not to overbrew green tea. While it's best to
follow the manufacturer's instructions for each variety of green tea, here are some
general instructions:
- Use one tea bag, or 2 - 4 grams of tea*, per cup.
- Fill a kettle with cold water and bring to a boil.
- After unplugging the kettle, allow it to stand for up to 3 minutes.
- Pour the heated water over the tea bag or tea, and allow it to steep for up to 3 minutes. If using a tea bag, remove the bag.
- Allow the tea to cool for three more minutes.
*One to two teaspoons, depending on the variety of green tea you are brewing.
http://en.wikipedia.org/wiki/Green_tea
http://chinesefood.about.com/library/weekly/aa011400a.htm
http://www.theteacentre.com.au/pages/GREEN-TEA-%E2%80%93-MIRACLE-CURE.html
Nigella sativa "Black Seeds"
Nigella sativa is an annual flowering plant, native to south and southwest Asia. It grows to 20–30 cm (7.9–12 in) tall, with finely divided, linear (but not thread-like) leaves.
History of medicine
In the Unani Tibb system of medicine, black cumin is regarded as a valuable remedy for a number of diseases. Sayings of the Islamic prophet Muhammad underline the significance of black cumin. According to a hadith narrated by Abu Hurairah, he says, "I have heard the Messenger of Allah, saying that the black granules (kalonji) is the remedy for all diseases except death."
The seeds have been traditionally used in the Middle East and Southeast Asian countries for a variety of ailments. In modern Marrakech, nigella seeds are sold in small bundles to be rubbed until warm, when they emit an aroma which opens clogged sinuses in the way that do eucalyptus or Vicks.
Nestlé has filed a patent application covering use of Nigella sativa as a food allergy treatment.
Medical studies
Thymoquinone, found in the seed oil extract of N. sativa, has been shown to have anti-neoplastic effects in rats and mice and in cultured human cells from several types of cancer, including pancreatic ductal adenocarcinoma. It has protective antioxidant and anti-inflammatory effects, and promotes apoptosis (cell death) of the cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/12722128
http://en.wikipedia.org/wiki/Nigella_sativa
http://www.mskcc.org/cancer-care/integrative-medicine/disclaimer?msk_disclaimer_herb=1&destination=%2Fcancer-care%2Fherb%2Fnigella-sativa
Monday, 22 July 2013
Aids - Everything you need to know
When you get infected with the HIV virus, you can get AIDS, which stands for 'acquired immune deficiency syndrome'. This means that you have a deficient immune system. This animation explains how you can get infected with the HIV virus and what it means when you are 'sero positive'. It also explains the different disease stages and possible treatment options.
Sunday, 21 July 2013
Saturday, 20 July 2013
The Invisible World
We are all surrounded by The Invisible World microorganisms, they live on us within us and around us, they affect everything we do, yet most people have no idea what they look like. Using the latest technology it is possible to see into this normally invisible world
Friday, 19 July 2013
Intermittent Fasting and Longevity
Intermittent fasting (IF) is a pattern of eating that alternates between periods of fasting (usually meaning consumption of water and sometimes low-calorie drinks such as black coffee) and non-fasting.
There is evidence suggesting that intermittent fasting may have beneficial effects on the health and longevity of animals—including humans—that are similar to the effects of caloric restriction
(CR). There is currently no consensus as to the degree to which this is
simply due to fasting or due to an (often) concomitant overall decrease
in calories, but recent studies have shown support for the former.[1][2] Alternate-day calorie restriction may prolong life span.[3]
Intermittent fasting and caloric restriction are forms of dietary
restriction (DR), which is sometimes referred to as dietary energy
restriction (DER).
Scientific study of intermittent fasting in rats (and anecdotally in humans) was carried out at least as early as 1943.[4]
A specific form of intermittent fasting is alternate day fasting (ADF), also referred to as every other day fasting (EOD), or every other day feeding (EODF), a 48-hour routine typically composed of a 24-hour fast followed by a 24-hour non-fasting period.
Insulin-like growth factor is produced in the liver and released
according to activity of Human Growth Hormone (HGH), produced in the
pituitary gland. Levels of both naturally decline with age, which is
desirable: high levels of IGF-1 encourage the body to focus on producing
new cells rather than existing repairing ones. As cellular and DNA
damage continues to go unchecked, aging and disease take hold. What's
more, cancerous cells usually mutate to take advantage of both insulin
and IGF-1, using them as fuel. The reverse is also true: in mice
genetically engineered to have low levels of IGF-1, lifespan increases
to the human equivalent of 120 years, and among the few hundred people
worldwide with low IGF-1, cancer and diabetes are virtually unknown.
In the recent BBC documentary "Eat, Fast and Live Longer," Michael Mosley fasted for three days and four nights. The result? Halved levels of IGF-1, slashing his risk for age-related disease. His blood glucose levels also fell, indicating improved sensitivity to insulin and lessened risk of developing diabetes. As is typical, after returning to his normal diet Mosley's IGF-1 levels rose to what they were before. To maintain lower levels of the hormone, Mosley adopted the practice of intermittent fasting, taking up what is known as the 5:2 diet. Followers of the 5:2 diet eat whatever they want five days a week and about 500 calories twice a week. Amazingly, following this simple formula is known to lower blood pressure, HDL cholesterol and blood lipids and sustain weight loss no matter what kind of food is consumed. After five weeks on the diet, Mosley lost almost 15 pounds.
Additional promising research on mice suggests that intermittent fasting protects against mental illnesses including Alzheimer's, Parkinson's and dementia.
Two simpler dietary interventions also promise some dampening of IGF-1: lowering protein intake, which for most people is higher than is optimal, and refraining from milk. Hormone-rich milk contains an abundance of IGF-1 and is known to contribute to the risk of cancer, particularly fatal prostate cancer.
Microarray analyses identify fasting-regulated genes involved in IF-induced longevity
a, The sampling scheme is shown. b, d, Expression profiles of fasting-induced up-regulated (b, left) and down-regulated (d) genes. Average expression profiles are shown (b, right, see text). c, Scatter plots of the expression levels for TOR (let-363) RNAi-fasting (top left) or rheb-1
RNAi-fasting (top right) worms. The black and blue lines indicate the
diagonal and twofold changes between two samples. Venn diagram of
fasting-induced 112 genes (bottom). e, Quantitative PCR with reverse transcription (qRT–PCR) of ins-7 expression. f, HSP-12.6, a downstream target of DAF-16, functions to mediate IF-induced longevity.
- Anson, R. Michael; Guo, Zhihong; de Cabo, Rafael; Iyun, Titilola; Rios, Michelle; Hagepanos, Adrienne; Ingram, Donald K.; Lane, Mark A. et al. (2003). "Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake". Proceedings of the National Academy of Sciences 100 (10): 6216–20. Bibcode:2003PNAS..100.6216A. doi:10.1073/pnas.1035720100. JSTOR 3147568. PMC 156352. PMID 12724520.
- Wan, R; Camandola, S; Mattson, MP (2003). "Intermittent food deprivation improves cardiovascular and neuroendocrine responses to stress in rats". The Journal of nutrition 133 (6): 1921–9. PMID 12771340.
- Johnson, James B.; Laub, Donald R.; John, Sujit (2006). "The effect on health of alternate day calorie restriction: Eating less and more than needed on alternate days prolongs life". Medical Hypotheses 67 (2): 209–11. doi:10.1016/j.mehy.2006.01.030. PMID 16529878.
- Carlson, AJ; Hoelzel, F (1946). "Apparent prolongation of the life span of rats by intermittent fasting". The Journal of nutrition 31: 363–75. PMID 21021020.
- en.wikipedia.org/wiki/Intermittent_fasting#cite_note-pmid12724520-1
- http://www.naturalnews.com/037474_intermittent_fasting_longevity_igf-1.html
Intestinal bacteria are linked to white blood cell cancer
Researchers from UCLA's Jonsson Comprehensive Cancer Center (JCCC)
have discovered that specific types of bacteria that live in the gut are
major contributors to lymphoma, a cancer of the white blood cells that
are part of the human immune system.
Researchers from UCLA's Jonsson Comprehensive Cancer Center have
discovered that specific types of bacteria that live in the gut are
major contributors to lymphoma, a cancer of the white blood cells.
Published online ahead of press today in the journal Cancer
Research, the study was led by Robert Schiestl, member of the Jonsson
Cancer Center and professor of pathology and laboratory medicine,
environmental health sciences, and radiation oncology.
In rodents, intestinal bacteria influence obesity, intestinal
inflammation and certain types of epithelial cancers. (Epithelial
cancers affect the coverings of the stomach, liver or colon.) However,
little is known about the identity of the bacterial species that promote
the growth of, or protect the body from, cancer — or about their effect
on lymphoma.
Up to 1,000 different species of bacteria (intestinal microbiota)
live in the human gut. Intestinal microbiota number 100 trillion cells;
over 90 percent of the cells in the body are bacteria. The composition
of each person's microbiome — the body's bacterial make-up — is very
different, due to the types of bacteria people ingest early in their
lives, as well as the effects of diet and lifestyle.
Schiestl's group wanted to determine whether differences in
peoples' microbiomes affect their risk for lymphoma, and whether
changing the bacteria can reduce this risk. They studied mice with
ataxia-telangiectasia (A-T), a genetic disease that in humans and mice
is associated with a high rate of B-cell lymphoma. They discovered that,
of mice with A-T, those with certain microbial species lived much
longer than those with other bacteria before developing lymphoma, and
had less of the gene damage (genotoxicity) that causes lymphoma.
"This study is the first to show a relationship between intestinal
microbiota and the onset of lymphoma," Schiestl said. "Given that
intestinal microbiota is a potentially modifiable trait, these results
hold considerable promise for intervention of B-cell lymphoma and other
diseases."
The scientists also were able to create a detailed catalog of
bacteria types with promoting or protective effects on genotoxicity and
lymphoma, which could be used in the future to create combined therapies
that kill the bacteria that promote cancer (as antibiotics do) and
increase the presence of the bacteria that protect from cancer (as
probiotics do).
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Immunology II. INNATE IMMUNITY
INNATE IMMUNITY
A. Innate immunity includes defenses (physical, chemical, and cellular) that are poised to either prevent an infection or act rapidly to an infection. Innate defenses do not need prior exposure to an antigen to respond.
B. Anatomic and mechanical barriers to infection are designed to prevent infectious agents from accessing the body and include the skin, which is covered by protective layers of keratinized cells; mucus, which provides a mechanical and chemical barrier to infection; and chemical and molecular factors, such as surfactants, low pH, high salt, and acids. Some of these factors (low pH, high salt, surfactants, and acid) interfere directly with microbial life, whereas others recognize features of microbes that are common to some or all microbes (e.g., the enzyme lysozyme, which is found in tears, saliva, gastric secretions, and lysosomal granules of phagocytes, cleaves peptidoglycan of bacterial cell walls).
Defensins and cathelicidins are small cationic antimicrobial peptides that have direct antimicrobial activity, are found at mucosal surfaces, and are produced by many immune cells. Interferons, which interfere with viral replication, are released by host cells or immune cells in response to the presence of intracellular viruses. Biological factors such as normal flora bacteria (especially on the skin and gastrointestinal tract surfaces) provide a defense against infection by physically preventing access to the surfaces of the body, producing metabolites that create an inhospitable environment for pathogens, and consuming available nutrients.
C. Phagocytosis is the process by which microbes are engulfed and destroyed by immune cells, usually neutrophils or macrophages. Phagocytes can recognize some microbes directly (further discussed later).
D. The complement system consists of approximately 30 circulating and membrane-expressed proteins that serve as an effector system of both the innate and antibody-mediated adaptive immune responses.
Most of the complement components are synthesized in an inactive form by the liver, and then activated, in a cascade manner, when needed. Complement activation occurs through three different pathways: alternative, classical, and lectin. Complement is responsible for increases in the inflammatory response, opsonization to enhance phagocytosis, lysis of cells, and immune complex clearance. Regardless of the mechanism of activation, all three pathways converge at C3, which is the most abundant complement protein in the blood.
1. Complement activation
a. The alternative pathway of complement activation is triggered by the carbohydrates, lipids, and proteins that are often found on foreign surfaces, particularly bacteria and fungi. The precipitating event involves spontaneous hydrolysis of complement C3 followed by C3b covalently binding to nearby surfaces. Other complement components then associate to continue the cascade of activation.
b. The classical pathway is initiated by the association of complement component C1 with immune complexes containing IgG or IgM. Alternatively, C1 can bind to several pentraxin proteins that are synthesized in response to infection, including pentraxin 3 (PTX3) and the acute-phase proteins—C-reactive protein (CRP) and serum amyloid P-component (SAP). Binding of C1 then activates other complement components to continue the cascade of activation.
c. The lectin pathway is activated when the mannose-binding lectin (MBL) binds to the carbohydrate moieties found on the surface of many bacteria, fungi, and parasites. Binding of MBL induces a conformational change such that MBL-associated proteins are active to continue the cascade of activation.
1. Complement activation
a. The alternative pathway of complement activation is triggered by the carbohydrates, lipids, and proteins that are often found on foreign surfaces, particularly bacteria and fungi. The precipitating event involves spontaneous hydrolysis of complement C3 followed by C3b covalently binding to nearby surfaces. Other complement components then associate to continue the cascade of activation.
b. The classical pathway is initiated by the association of complement component C1 with immune complexes containing IgG or IgM. Alternatively, C1 can bind to several pentraxin proteins that are synthesized in response to infection, including pentraxin 3 (PTX3) and the acute-phase proteins—C-reactive protein (CRP) and serum amyloid P-component (SAP). Binding of C1 then activates other complement components to continue the cascade of activation.
c. The lectin pathway is activated when the mannose-binding lectin (MBL) binds to the carbohydrate moieties found on the surface of many bacteria, fungi, and parasites. Binding of MBL induces a conformational change such that MBL-associated proteins are active to continue the cascade of activation.
2. Defensive functions of complement. In the initial stages of the complement cascade, individual components are cleaved into fragments (typically designated by lowercase letters) that sequentially generate biologically active molecules. Because one active complement molecule can act on multiple subsequent complement molecules, initially small-initiating signals can be rapidly amplified.
a. Opsonins produced by complement, chiefly C3b, are covalently attached to the target surface. Phagocytic cells that have receptors for C3b include neutrophils and resident tissue macrophages.
b. Anaphylatoxins (potent activators of inflammation) are peptides (C3a and C5a) that exert their effects by binding to receptors present on a number of different cell types. Anaphylatoxins act as chemoattractants for phagocytes, stimulate vasodilation and smooth muscle contraction, and induce histamine release and oxidative burst in mast cells and neutrophils, respectively.
c. The membrane attack complex (MAC), formed by complement components C5b678 and polymerized subunits of C9, lyses target cells by forming a pore in the target cell membrane.
d. Complement activation through the classical pathway is an important feature of immune complex clearance. Small immune complexes, consisting of antigen–antibody (IgG or IgM) and C3b, are efficiently bound to the complement receptors present on erythrocytes and are then removed from the surface of the erythrocyte in the liver and spleen.
e. Regulatory proteins present on the membrane of the host cell (complement receptor 1, membrane co-factor protein(CD46), decay accelerating factor, and CD59) or as soluble proteins in the plasma (factor I and factor H) act at different steps of the complement cascade to prevent the inappropriate activation of complement on host cells and tissues.
E. The acute-phase response (APR) is a coordinated response to a number of triggers, including proinflammatory cytokines and bacterial LPS. During the APR, the hepatic production of a number of proteins is increased, including complement factors such as C3, MBL, and C-reactive protein; coagulation factors such as fibrinogen, plasminogen, and tissue plasminogen activator; transport and metal-binding proteins; and immunomodulatory agents such as granulocyte colony-stimulating factor and IL-1 receptor antagonist.
F. Inflammation is a collection of events that rapidly occurs following tissue injury or infection. There are several inflammatory pathways; many of the individual steps of inflammation are controlled by cytokines or other small regulatory molecules that are often referred to as inflammatory mediators.
The inflammatory response is largely protective, although in certain circumstances, such as hypersensitivity reactions and autoimmune diseases, inflammation can be the major mechanism of harm to the body. The hallmark signs of inflammation are pain, redness, swelling, and heat, most of which can be attributed to vasodilation of the local blood vessels, increased local vascular permeability (edema), and the inflammatory mediators that assist with leukocyte transmigration from the circulation to the tissue.
G. Phagocytic cells (neutrophils and monocytes/macrophages) are important cells of the innate immune defense system.
1. The phagocytes are recruited to sites of inflammation by adhesions that are expressed on local endothelial cells. The phagocytes then migrate to the site of the infection by following the concentration of inflammatory mediators.
2. Phagocytic cells can engulf bacteria, cellular debris, and other particulate matter via a number of recognition mechanisms. Neutrophils and macrophages also have a number of pattern recognition receptors (PRRs) that can bind directly to pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide, peptidoglycan, lipoteichoic acids, and mannans, which are widely expressed by microbial pathogens as repetitive motifs but are not present on host cells or tissues. Phagocytes also have receptors to bind to opsonins, such as antibody and complement.
3. Components that have been engulfed by a neutrophil or macrophage are initially contained within a membrane-bound vesicle, which then fuses with cytoplasmic granules containing defensins, lysozyme, lactoferrin, proteases, and other enzymes. The cell also acidifies the vesicle by actively pumping hydrogen ions into the interior. Phagocytes also synthesize a number of powerful oxidizing agents (superoxide anion, hydrogen peroxide, and hydroxyl radicals) via oxidative pathways (respiratory burst or oxidative burst).
1. The phagocytes are recruited to sites of inflammation by adhesions that are expressed on local endothelial cells. The phagocytes then migrate to the site of the infection by following the concentration of inflammatory mediators.
2. Phagocytic cells can engulf bacteria, cellular debris, and other particulate matter via a number of recognition mechanisms. Neutrophils and macrophages also have a number of pattern recognition receptors (PRRs) that can bind directly to pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide, peptidoglycan, lipoteichoic acids, and mannans, which are widely expressed by microbial pathogens as repetitive motifs but are not present on host cells or tissues. Phagocytes also have receptors to bind to opsonins, such as antibody and complement.
3. Components that have been engulfed by a neutrophil or macrophage are initially contained within a membrane-bound vesicle, which then fuses with cytoplasmic granules containing defensins, lysozyme, lactoferrin, proteases, and other enzymes. The cell also acidifies the vesicle by actively pumping hydrogen ions into the interior. Phagocytes also synthesize a number of powerful oxidizing agents (superoxide anion, hydrogen peroxide, and hydroxyl radicals) via oxidative pathways (respiratory burst or oxidative burst).
H. Toll-like receptors (TLRs) are a family of pattern-recognition receptors of innate immunity that are present on many types of leukocytes, especially macrophages, dendritic cells, and neutrophils. Each type of TLR is specific for a different type of common pathogen component, such as lipopolysaccharide, teichoic acid, flagellin, and double-stranded RNA. TLRs share structural homology to each other and are membrane associated, being associated with either the outer membrane or internal membrane structures, depending on the PAMP that they recognize. Upon binding, TLRs induce phagocyte activation, enable the initiation of the adaptive immune response, and elicit the production of various cytokines for further immune function.
Ref:
Comprehensive Pharmacy Review
Wikipedia
Some pictures in this article are found by google search; http://textbookofbacteriology.net/imgcid.jpg
http://upload.wikimedia.org/wikipedia/commons/a/a9/Innate_immune_system.png
http://www.redorbit.com/media/gallery/national-science-foundation-gallery/medium/183_5bf1fec06e7f7f091adedd6bc640677d.jpg
http://upload.wikimedia.org/wikipedia/commons/b/b0/Complement-pathways.png
http://upload.wikimedia.org/wikipedia/commons/a/a9/Innate_immune_system.png
http://www.redorbit.com/media/gallery/national-science-foundation-gallery/medium/183_5bf1fec06e7f7f091adedd6bc640677d.jpg
http://upload.wikimedia.org/wikipedia/commons/b/b0/Complement-pathways.png
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Oral Probiotics
Probiotics are live microorganisms (e.g., bacteria) that are either
the same as or similar to microorganisms found naturally in the human
body and may be beneficial to health. Also referred to as “good
bacteria” or “helpful bacteria,” probiotics
are available to consumers in oral products such as dietary supplements
and yogurts, as well as other products such as suppositories and
creams. The U.S. Food and Drug Administration (FDA) has not approved any
health claims for probiotics. This fact sheet provides a general
overview of probiotics, with an emphasis on oral products, and suggests
sources for additional information.
The concept behind probiotics was introduced in the early 20th
century, when Nobel laureate Elie Metchnikoff, known as the “father of
probiotics,” proposed in The Prolongation of Life: Optimistic Studies
that ingesting microorganisms could have substantial health benefits
for humans. Microorganisms are invisible to the naked eye and exist
virtually everywhere. Scientists continued to investigate the concept,
and the term “probiotics”—meaning “for life”—eventually came into use.
Picturing the human body as a “host” for bacteria and other
microorganisms is helpful in understanding probiotics. The body,
especially the lower gastrointestinal tract (the gut), contains a
complex and diverse community of bacteria. (In the body of a healthy
adult, cells of microorganisms are estimated to outnumber human cells by
a factor of ten to one.) Although we tend to think of bacteria as
harmful “germs,” many bacteria actually help the body function properly.
Most probiotics are bacteria similar to the beneficial bacteria found
naturally in the human gut.
Various mechanisms may account for the effects of probiotics on human
health. Possible mechanisms include altering the intestinal
“microecology” (e.g., reducing harmful organisms in the intestine),
producing antimicrobial compounds (substances that destroy or suppress
the growth of microorganisms), and stimulating the body’s
immune response.
Probiotics commonly used in the United States include Lactobacillus and Bifidobacterium.
There are many specific types of bacteria within each of these two
broad groups, and health benefits associated with one type may not hold
true for others.
In the United States, probiotics are available as dietary supplements
(including capsules, tablets, and powders) and in dairy foods (such as
yogurts with live active cultures). According to the 2007 National
Health Interview Survey, which included a comprehensive survey on the
use of complementary health approaches by Americans,
“prebiotics/probiotics” ranked fifth among natural products used for
children, but were not among the top-ranking products for adults.
Although probiotic products are more popular in Europe and Japan than in
the United States, the U.S. consumer market for probiotics is
growing rapidly.
Although the FDA has not approved any health claims for probiotics,
they are used for a variety of gastrointestinal conditions such as
infectious diarrhea, diarrhea associated with using antibiotics,
irritable bowel syndrome, and inflammatory bowel disease (e.g.,
ulcerative colitis and Crohn’s disease). Probiotics are also being used
for preventing tooth decay and for preventing or treating other oral
health problems such as gingivitis and periodontitis. Some—but not
all—probiotic formulations have been widely studied and show
considerable promise. However, the rapid growth in marketing and
consumer interest and use has outpaced scientific research on the safety
and efficacy of probiotics for specific health applications.
The potential of probiotics to benefit human health in many different
ways has stimulated great interest and activity among researchers. For
example, the National Center for Complementary and Alternative Medicine
(NCCAM) is part of the National Institutes of Health (NIH) Probiotic and
Prebiotic Working Group, a trans-NIH effort to identify gaps and
challenges in prebiotic/probiotic research.
Probiotic research is moving forward on two fronts: basic science
(laboratory studies) and clinical trials to evaluate the safety and
efficacy of probiotics for various medical conditions. Many early
clinical trials of probiotics have had methodological limitations, and
definitive clinical evidence to support using specific probiotic strains
for specific health purposes is generally lacking. Nevertheless, there
is preliminary evidence for several uses of probiotics, and more studies
are under way. In particular, a recent review of the scientific
evidence on the effectiveness of probiotics in acute infectious diarrhea
concluded that there was evidence that probiotics may shorten the
duration of diarrhea and reduce stool frequency but that more research
was needed to establish exactly which probiotics should be used for
which groups of people.
In 2008, the journal Clinical Infectious Diseases published a
special issue on probiotics, which included an overview of clinical
applications. Based on a review of selected studies, the authors
classified several applications according to the strength of evidence
supporting the efficacy of probiotics in prevention and/or treatment.
For example, the authors concluded that strong evidence exists for acute
diarrhea and antibiotic-associated diarrhea, and substantial evidence
exists for atopic eczema (a skin condition most commonly seen in
infants). Promising applications include childhood respiratory
infections, tooth decay, nasal pathogens (bacteria harbored in the
nose), gastroenteritis relapses caused by Clostridium difficile
bacteria after antibiotic therapy, and inflammatory bowel disease. The
authors also discussed various potential future applications.
Studies also indicate that probiotics may reduce side effects associated with treatment for Helicobacter pylori
infection, the cause of most stomach ulcers. A systematic review
suggests that there is strong evidence that probiotics may reduce the
risk of necrotizing enterocolitis, a severe intestinal condition of
premature newborns. Other potential future applications include use in
reducing cholesterol levels, treating obesity, and managing irritable
bowel syndrome.
It appears that most people do not experience side effects from
probiotics or have only mild gastrointestinal side effects such as gas.
But there have been some case reports of serious adverse effects, and
research on safety is ongoing. A 2008 review of probiotics safety noted
that Lactobacillus rhamnosus GG has been widely studied in
clinical trials for a variety of conditions and generally found to be
safe. Nevertheless, a recent review of Lactobacillus and Bifidobacterium
noted that the long-term, cumulative effects of probiotics use,
especially in children, are unknown, and also pointed to evidence that
probiotics should not be used in critically ill patients. Similarly, a
2011 Agency for Healthcare Research and Quality assessment of the safety
of probiotics, partly funded by NCCAM, concluded that the current
evidence does not suggest a widespread risk of negative side effects
associated with probiotics. However, the data on safety, particularly
long-term safety, are limited, and the risk of serious side effects may
be greater in people who have underlying health conditions.
Concerns have also been raised about the quality of probiotic
products. Some products have been found to contain smaller numbers of
live microorganisms than expected. In addition, some products have been
found to contain bacterial strains other than those listed
as ingredients.
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Wednesday, 17 July 2013
Cannabis
Cannabis is a genus of flowering plants that includes three putative varieties, Cannabis sativa, Cannabis indica, and Cannabis ruderalis. These three taxa are indigenous to Central Asia, and South Asia.
Medical use
A synthetic form of the main psychoactive cannabinoid in Cannabis, tetrahydrocannabinol (THC), is used as a treatment for a wide range of medical conditions.
In the United States, although the Food and Drug Administration
(FDA) does acknowledge that "there has been considerable interest in
its use for the treatment of a number of conditions, including glaucoma,
AIDS wasting, neuropathic pain, treatment of spasticity associated with
multiple sclerosis, and chemotherapy-induced nausea," the agency has
not approved "medical marijuana". There are currently 2 oral forms of
cannabis (cannabinoids) available by prescription in the United States
for nausea and vomiting associated with cancer chemotherapy: dronabinol
(Marinol) and nabilone (Cesamet). Dronabinol is also approved for the
treatment of anorexia associated with AIDS. The FDA does facilitate scientific investigations into the medical uses of cannabinoids.
Medical cannabis is also used for analgesia,
or pain relief. It is also reported to be beneficial for treating
certain neurological illnesses such as epilepsy, and bipolar disorder. Case reports have found that Cannabis can relieve tics in people with obsessive compulsive disorder and Tourette syndrome. Patients treated with tetrahydrocannabinol, the main psychoactive chemical found in Cannabis, reported a significant decrease in both motor and vocal tics, some of 50% or more. Some decrease in obsessive-compulsive behavior was also found. A recent study has also concluded that cannabinoids found in Cannabis might have the ability to prevent Alzheimer's disease. THC has been shown to reduce arterial blockages.
http://medicalmarijuana.procon.org/
https://en.wikipedia.org/wiki/Cannabis
http://www.sciencedaily.com/releases/2013/04/130402124817.htm
Tuesday, 16 July 2013
Diphenhydramine
Diphenhydramine
Abbreviated DPH, sometimes DHM is a first-generation antihistamine possessing anticholinergic, antitussive, antiemetic, and sedative properties that is mainly used to treat allergies.
Medical uses
Diphenhydramine is a first-generation antihistamine used to treat a number of conditions including allergic symptoms and itchiness, the common cold, insomnia, motion sickness and extrapyramidal symptoms.
Diphenhydramine is significantly more potent in treatment of allergies than a newer generation of antihistamines. Consequently, it is frequently used when an allergic reaction requires fast, effective reversal of a massive histamine release. Diphenhydramine is available as an over-the-counter drug (OTC) or prescription-only solution for injection. Injectable diphenhydramine can be used for life-threatening reactions (anaphylaxis) to allergens such as bee stings, peanuts, or latex, as an adjunct to epinephrine
What side effects can this medication cause?
Diphenhydramine may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away:
-
dry mouth, nose, and throat
-
drowsiness
-
dizziness
-
nausea
-
vomiting
-
loss of appetite
-
constipation
-
increased chest congestion
-
headache
-
muscle weakness
-
excitement (especially in children)
- nervousness
- vision problems
-
difficulty urinating or painful urination
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682539.html
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