Body Detoxification
In reality, a person very rarely dies of cancer. It is always starvation and toxicity. As the malignant tumor grows it gives off waste products, which must be eliminated through the colon, liver, kidneys, lungs and skin. These waste products accumulate and gradually overburden the body. Most persons then die of toxemia. Before any disease can be cured, the waste products and impurities must be cleansed from the body. The sooner this is done, the sooner the body can begin repairing itself. The "detoxer" must be prepared to accept that there will be a "healing crisis." While on a cleanse the body will purge. The release of toxins will bring up physical and emotional trauma that will be reflected in certain symptoms. A healing crisis can last a few days and produce these symptoms: fever, headaches and other aches, fatigue, skin eruptions, emotional irritability, gas, temporary constipation or diarrhea, temporary loss of menstruation, yawning, and muscular tension. In most cases, it is important not to use drugs to suppress these symptoms, but instead, to encourage the release of toxins from the body. These symptoms are an expression of release and must come out
Importance of Zinc
Zinc is the transportation mechanism for laetrile and nitrilosides in the body. Biochemists and researchers have found that you can give Laetrile to a patient until its coming out of the ears of the patient, but, if that patient did not have sufficient level of Zinc, none of the laetrile would get into the tissues of the body. They also found that nothing heals within the body without sufficient Vitamin C. They also found that magnesium, selenium, vitamin A, and B all played an important part in maintaining the body's defence mechanism. This is why its very important to understand that cancer is best supported with a total nutritional program consisting of diet, vitamins, minerals, laetrile, and pancreatic enzymes.
One mechanism that cancer cells use to expand in the body is through digesting their surroundings. This mechanism was described by Dr. Matthius Rath in his book on cancer. Cancer cells produce and secrete millions of enzyme molecules, which, like scissors, cut collagen and tissue that surrounds cells. Cancer cells use these enzymes to cut little holes in the blood vessel wall and get into the blood stream where they can travel to other organs, such as the lungs. Using the same mechanism, cancer cells can settle there and start new tumor growth. This stage, called metastasis, is the most dangerous stage of cancer. If a tumor stays in one place it rarely endangers our life. But about 90% of cancer deaths are the result of metastases, when a tumor invades various organs in the body.
It must be natural mechanisms that keep cells in place and block the spread of cancer. Dr. Rath suggested that our bodies can use lysine, a natural amino acid, to block the action of collagen digesting enzymes. Research has shown that a combination of vitamin C with the natural amino-acids lysine, proline, and specific extracts from green tea will give support against the invasion of cancer cells. Lysine, like vitamin C, cannot be produced in our body. We can only get it from our diet, therefore, deficiency of lysine is likely. This means that our body's ability to control collagen digestion can be compromised if intake of lysine is too low. Food sources of lysine are numerous, but the richest sources include cheese, eggs, fish, lima beans, milk, potatoes, pork, poultry, red meat, soy products, yeast, all protein-rich foods. Vegetables are generally a poor source of lysine, with the exception of beans, peas, and lentils.
Dr. Rath uses the nutrient combination of vitamin C, the amino-acids L-lysine and L-proline, and Epigallocatechin Gallate ( EGCG - a polyphenol extract from green tea ) and has found these to be very effective in the nutritional support of the body. More good news... These same nutrients and same intake ( see below ) work well with cardiovascular disease. As a supportive measure against those who do not have cancer, heart attacks or strokes, cut intake ( below ) by 70% or 50% for those with family history of cancer, heart attack or stroke which are considered high risk.
Note: The beneficial effects is reportedly much more pronounced and immediate when sugar and refined carbohydrates is eliminated. Sugar feeds cancer and sugar can crowd out vitamin C.
Eating the normal western diet is a recipe for disaster for the cancer patient. Poor nutrition provides a favorable environment for cancer to grow and develop. Proper nutrition supports the immune system, starves cancer cells, and helps maintain the body at a normal, slightly alkaline pH - 7.35 to 7.45. Disease cannot survive in an oxygen rich alkaline state. The only place in your body where there is no oxygen is the cancer site. The best way to raise body pH is making sure that adequate minerals, particularly calcium are present. In general, green vegetables are high in calcium. One of the quickest ways to raise your body pH is to take in green vegetable juices. Kale, broccoli, and collard greens are good sources of calcium, buy a juicer and start juicing. The juicer is the most important appliance in the kitchen for the cancer patient. As nutritional support, the best choice is a combination of water fasting and juice fasting using 2 to 5 glasses of juice per day.
So if we are going to purchase a juicer, should we buy a centrifugal or a mastication-type juicer? At the Gerson Clinic in Mexico, they are the most knowledgeable people we know to ask what kind of juicer works best. So what do they teach? They teach that only mastication-type juicers will do the job because centrifugal juicers leave most of the nutrients in the pulp, which then gets thrown away. ( The laboratory report where they ran five pounds of carrots through a centrifugal juicer and a mastication-type juicer, and the mastication-type juicer removed three to four times more nutrients than the centrifugal ). The mastication-type juicer leaves very few nutrients in the pulp. For this reason, we recommend only mastication juicers for the cancer patient.
29 April 2008
Spermatogenesis
Sperm are among the most highly specialized cell types ever described. Such specialization is designed to get the sperm to the egg and to fuse with it. The testes are sperm factories, which produce vast numbers of these elaborate cells.
Germ Cell - Somatic Cell Interactions
Sperm develop in association with specialized somatic cells. Mammalian testes contain numerous seminiferous tubules. Sertoli cells are radially distributed around the circumference of the seminiferous tubules. Spermatogonia are located between the Sertoli cells and the basal lamina. As their progeny undergo meiosis and spermiogenesis (differentiation), they are translocated in groups around the circumference of the seminal tubule toward the lumen. Thus, one sees circumferential zones of more advanced cells inside zones of less advanced cells.
This translocation is mediated by the Sertoli cells. When the differentiated spermatozoa reach the tips of the Sertoli cells, they are released into the lumen of the tubule. Tight junctions are formed between adjacent Sertoli cells, producing a diffusion barrier, allowing the Sertoli cells to regulate the environment that bathes the germ cells.
Regulating Spermatogenesis
The coordination of most developmental processes requires a system of extracellular signals to control cellular survival and proliferation, specification of cell fate, patterning and promotion of cell differentiation. Signaling mechanisms require a signal source, a signal reception system and an intracellular signal response system. Signals that originate from a distance and are distributed via the circulation are called endocrine signals or hormones. Signals coming from nearby cells are called paracrine signals. Cells can also signal themselves; such signals are autocrine signals. These various kinds of signals help to insure that development occurs in an orderly way.The major players that regulate mammalian spermatogenesis are:Androgens (e.g., testosterone), which are secreted by the Leydig (interstitial) cells, which are located in the connective tissue between the seminiferous tubules.Luteinizing hormone (LH) and follicle stimulating hormone (FSH), which are released from the pituitary under the control of gonadotropin-releasing hormone (GnRH), from the hypothalamus. Androgens in the circulation cause a reduction in the production of LH under a classical feedback-inhibition mechanism. Germ cells lack FSH receptors, but Sertoli cells have them. One effect of FSH on Sertoli cells is to cause them to secrete androgen-binding protein, which binds to androgens and may facilitate their direct effects on germ cell differentiation. Growth Factors. Growth factors are proteins that bind to receptors in the surface of target cells and either stimulate cell division or alter cell fate.Sertoli cells produce a number of growth factors of significance. One is seminiferous growth factor (SGF), which stimulates somatic cell proliferation and blood vessel production in the testis during fetal and postnatal development. In the adult, Sertoli cells respond to their own production of SGF by producing sulfated glycoprotein-2 (SGP-2). This is an autocrine interaction. What mechanism would allow a Sertoli cell to respond to its own secretory product? SGP-2 is the major secretory product of adult Sertoli cells. It, in turn, binds to the membranes of spermatozoa. This is a paracrine interaction.Another growth factor is inhibin, which is released from Sertoli cells into the circulation and functions to suppress the secretion of FSH from the pituitary . Circulating levels of FSH, in turn, regulate inhibin production, indicating that a classical negative-feedback mechanism operates. Inhibin is a member of the TGF-ß superfamily of growth factors. Inhibins are heterodimeric proteins (i.e., they are composed of two different polypeptides) of an alpha chain and a beta chain. A related growth factor is activin, which consists of two beta chains. (Activin has been implicated in embryonic induction.)Another category of TGF-ß molecules of significance for spermatogenesis is the bone morphogenetic protein (BMP) family. This is a diverse family of secreted signaling molecules, whose members are involved in controlling a variety of developmental processes. TGF-ß receptors are expressed in the mammalian testis, suggesting that members of the TGF-ß family of signaling molecules play a role in spermatogenesis. At least one member of this family, BMP8b, which is produced within the germ cells themselves, is essential for spermatogenesis in mice. The requirement for BMP8b for spermatogenesis has been demonstrated by the gene knock-out technique. This technique enables investigators to selectively eliminate specific genes and assess the consequences. Testes of the mutant mice show two distinct effects. During early puberty, the germ cells show either a failure or reduced capacity for proliferation and delayed differentiation. In adults, the spermatocytes have a significantly elevated incidence of programmed cell death (apoptosis), which leads to depletion of the germ cells and, consequently, sterility.
Neomycin
Neomycin was discovered in 1949 by the microbiologist Selman Waksman and his student Hubert Lechevalier. It is produced naturally by the bacterium Streptomyces fradiae.
Neomycin is an aminoglycoside antibiotic that is found in many topical medications such as creams, ointments and eyedrops.
Formula C23H46N6O13 Mol. mass 614.644 g/mol
Half life 2 to 3 hours
Drug Uses
Neomycin is overwhelmingly used as a topical preparation. It can also be given orally, where it is usually combined with other antibiotics. Neomycin is not absorbed from the gastrointestinal tract, and has been used as a preventative measure for hepatic encephalopathy and hypercholesterolemia. By killing bacteria in the intestinal tract, it keeps ammonia levels low and prevents hepatic encephalopathy, especially prior to GI surgery. It has also been used to treat small intestinal bacterial overgrowth. It is not given intravenously, as neomycin is extremely nephrotoxic (causes kidney damage), especially compared to other aminoglycosides. The exception to this, is when it is included in some vaccines as a preservative, but in very small quantities -typically 0.025 mg per dose.
Neomycin is now also used in certain cell culture applications.
Drug Spectrum
Similar to other aminoglycosides, neomycin has excellent activity against Gram negative bacteria, and has partial activity against Gram positive bacteria. It is relatively toxic to humans, and many people have allergic reactions to it. See: Hypersensitivity. Physicians sometimes recommend using antibiotic ointments wihout neomycin, such as Polysporin.
Neomycin is an aminoglycoside antibiotic that is found in many topical medications such as creams, ointments and eyedrops.
Formula C23H46N6O13 Mol. mass 614.644 g/mol
Half life 2 to 3 hours
Drug Uses
Neomycin is overwhelmingly used as a topical preparation. It can also be given orally, where it is usually combined with other antibiotics. Neomycin is not absorbed from the gastrointestinal tract, and has been used as a preventative measure for hepatic encephalopathy and hypercholesterolemia. By killing bacteria in the intestinal tract, it keeps ammonia levels low and prevents hepatic encephalopathy, especially prior to GI surgery. It has also been used to treat small intestinal bacterial overgrowth. It is not given intravenously, as neomycin is extremely nephrotoxic (causes kidney damage), especially compared to other aminoglycosides. The exception to this, is when it is included in some vaccines as a preservative, but in very small quantities -typically 0.025 mg per dose.
Neomycin is now also used in certain cell culture applications.
Drug Spectrum
Similar to other aminoglycosides, neomycin has excellent activity against Gram negative bacteria, and has partial activity against Gram positive bacteria. It is relatively toxic to humans, and many people have allergic reactions to it. See: Hypersensitivity. Physicians sometimes recommend using antibiotic ointments wihout neomycin, such as Polysporin.
Furosemid
Drug Indications
Edema, due to cardiac, hepatal and renal diseases; preeclamsia and eclamsia edema; chronic cardiovascular failure; swelling in burns; arterial hypertension (when saluretics are contraindicated); in intoxications, in order to cause forced diuresis; in complex treatment of the pulmonary and intracranial edema.
Drug Contraindications
Severe liver failure (hepatal coma); acute intoxication with salicilate; renal failure, accompanied by anuria or oliguria; severe hypokaliemia; hypovolemia with or without hypotension.
Special warnings and precautions
Before the treatment with Furosemid existing hypokalemia, hyponatremia, hypovolemia and hypotension should be corrected. During the treatment a potassium-rich diet is advisable. Furosemid should be used with care in patients with auditory disorders, allergy to sulphonamydes, and micturiton disorders. In pregnant women Furosemid should be administered only after precise indications consideration. It should be kept in mind that in nursing women the preparation passes in the mother milk and depresses lactation. In such cases is advisable to stop the nursing. In drivers and machinery operating persons Furosemid may disturb capabilities to normal professional activity.
Drug interactions
Furosemid reduces the therapeutic effect of vasopressor amines and anti-diabetic medicines; potentiates the nephrotoxic effect of the cephalosporins, the ototoxic effect of aminoglycosides, and cardio- and neurotoxic effects of the lithium; potentiates effects of antihypertensive drugs and tubocurarine. In combined treatment with cardiac glycosides the preparation increases sensitivity of the myocardium to digitalis. In concomitant treatment with high dose salicylates salicylate intoxication is possibly to develop. Indometacin reduces diuretic and antihypertensive effects of Furosemid.
Adverse reactions
In high dose hypokalemia, hyponatremia, hypocalcemia, hypovolemia, dehydration, thrombosis and other violation of water-electrolyte balance may develop; in predisposed patients allergy skin rash may be seen; blood count changes (leucopenia, agranulocytosis, thrombocytopenia). In elderly patients with high dosesis is possibly to develop a circulatory collapse.
Pharmacological mechanisms
Furosemide exerts a powerful diuretic effect, causing a high (20-30%) glomerular excretion of sodium and water. It acts on the medullar portion of the ascending limb of Henle loop, where are absorbed chloride and sodium ions, but not water, blocking predominantly the active chloride transport. The sodium reabsorption inhibition is a secondary effect. The preparation increases the selective elimination of the sodium up to 35%, and, depending on the dose, stimulates renin - angiotensin - aldosterone system. This leads to reducing of the cortical-papillary osmotic gradient and significant decrease of the concentration capabilities of the kidney. Before the diuretic effect become evident Furosemid reduces the heart preload by dilation of the capacitive vessels, in case the renal function is normal and no significant edemas exist.
From : http://www.sopharma.com/
Edema, due to cardiac, hepatal and renal diseases; preeclamsia and eclamsia edema; chronic cardiovascular failure; swelling in burns; arterial hypertension (when saluretics are contraindicated); in intoxications, in order to cause forced diuresis; in complex treatment of the pulmonary and intracranial edema.
Drug Contraindications
Severe liver failure (hepatal coma); acute intoxication with salicilate; renal failure, accompanied by anuria or oliguria; severe hypokaliemia; hypovolemia with or without hypotension.
Special warnings and precautions
Before the treatment with Furosemid existing hypokalemia, hyponatremia, hypovolemia and hypotension should be corrected. During the treatment a potassium-rich diet is advisable. Furosemid should be used with care in patients with auditory disorders, allergy to sulphonamydes, and micturiton disorders. In pregnant women Furosemid should be administered only after precise indications consideration. It should be kept in mind that in nursing women the preparation passes in the mother milk and depresses lactation. In such cases is advisable to stop the nursing. In drivers and machinery operating persons Furosemid may disturb capabilities to normal professional activity.
Drug interactions
Furosemid reduces the therapeutic effect of vasopressor amines and anti-diabetic medicines; potentiates the nephrotoxic effect of the cephalosporins, the ototoxic effect of aminoglycosides, and cardio- and neurotoxic effects of the lithium; potentiates effects of antihypertensive drugs and tubocurarine. In combined treatment with cardiac glycosides the preparation increases sensitivity of the myocardium to digitalis. In concomitant treatment with high dose salicylates salicylate intoxication is possibly to develop. Indometacin reduces diuretic and antihypertensive effects of Furosemid.
Adverse reactions
In high dose hypokalemia, hyponatremia, hypocalcemia, hypovolemia, dehydration, thrombosis and other violation of water-electrolyte balance may develop; in predisposed patients allergy skin rash may be seen; blood count changes (leucopenia, agranulocytosis, thrombocytopenia). In elderly patients with high dosesis is possibly to develop a circulatory collapse.
Pharmacological mechanisms
Furosemide exerts a powerful diuretic effect, causing a high (20-30%) glomerular excretion of sodium and water. It acts on the medullar portion of the ascending limb of Henle loop, where are absorbed chloride and sodium ions, but not water, blocking predominantly the active chloride transport. The sodium reabsorption inhibition is a secondary effect. The preparation increases the selective elimination of the sodium up to 35%, and, depending on the dose, stimulates renin - angiotensin - aldosterone system. This leads to reducing of the cortical-papillary osmotic gradient and significant decrease of the concentration capabilities of the kidney. Before the diuretic effect become evident Furosemid reduces the heart preload by dilation of the capacitive vessels, in case the renal function is normal and no significant edemas exist.
From : http://www.sopharma.com/
28 April 2008
Metronidazole : DRUGS-HEALTH
Metronidazole is an antibiotic. Metronidazole is used to treat bacterial infections of the vagina, stomach, skin, joints, and respiratory tract. This medication will not treat a vaginal yeast infection but may also be used for other purposes not listed in this medication guide.
Important about metronidazole
Take this medication for the entire length of time prescribed by your doctor. Your symptoms may get better before the infection is completely treated. Metronidazole will not treat a viral infection such as the common cold or flu. Do not drink alcohol while you are taking metronidazole and for at least 3 days after you stop taking it. You may have unpleasant side effects such as fast heartbeats, warmth or redness under your skin, tingly feeling, nausea, and vomiting.
Before taking metronidazole
Tell your doctor if you are pregnant or plan to become pregnant during treatment.
Before taking metronidazole, tell your doctor if you are allergic to any drugs, or if you have: Liver disease; a stomach or intestinal disease such as Crohn's disease; a blood cell disorder such as anemia (lack of red blood cells) or leukopenia (lack of white blood cells); epilepsy or other seizure disorder; or nerve disorders.
If you have any of these conditions, you may need a dose adjustment or special tests to safely take this medication. Metronidazole can pass into breast milk and may harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.
How should I take metronidazole?
Take this medication exactly as it was prescribed for you. Do not take the medication in larger amounts, or take it for longer than recommended by your doctor. Follow the directions on your prescription label. Take the extended-release form of metronidazole on an empty stomach, at least 1 hour before or 2 hours after eating a meal. Do not crush, chew, or break the extended-release tablet. Swallow the pill whole. It is specially made to release medicine slowly in the body. Breaking the pill would cause too much of the drug to be released at one time. Take this medication for the entire length of time prescribed by your doctor. Your symptoms may get better before the infection is completely treated. Metronidazole will not treat a viral infection such as the common cold or flu.
To be sure this medication is not causing harmful effects, your blood will need to be tested on a regular basis. Your liver function may also need to be tested. Do not miss any scheduled visits to your doctor.
This medication can cause you to have unusual results with certain medical tests. Tell any doctor who treats you that you are using metronidazole. Store metronidazole at room temperature away from moisture and heat.
What happens if I miss a dose?
Take the missed dose as soon as you remember. If it is almost time for your next dose, skip the missed dose and take the medicine at your next regularly scheduled time. Do not take extra medicine to make up the missed dose.
What happens if I overdose?
Seek emergency medical attention if you think you have used too much of this medicine.
Overdose symptoms may include nausea, vomiting, dizziness, loss of balance or coordination, numbness and tingling, or seizures (convulsions).
What should I avoid while taking metronidazole?
Do not drink alcohol while you are taking metronidazole and for at least 3 days after you stop taking it. You may have unpleasant side effects such as fast heartbeats, warmth or redness under your skin, tingly feeling, nausea, and vomiting.
Check the labels of any medicines or food products you use to make sure they do not contain alcohol. Antibiotic medicines can cause diarrhea, which may be a sign of a new infection. If you have diarrhea that is watery or has blood in it, call your doctor. Do not use any medicine to stop the diarrhea unless your doctor has told you to.
Metronidazole side effects
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Call your doctor at once if you have any of these serious side effects:
Seizures (convulsions); fever, chills, body aches, sore throat, flu symptoms; numbness or tingling in your hands or feet; white patches or sores inside your mouth or on your lips; pain or burning when you urinate; or diarrhea that is watery or bloody.
Less serious side effects may include:
Nausea, stomach pain, diarrhea; headache, dizziness, loss of balance; vaginal itching or discharge; dry mouth or unpleasant metallic taste; cough, sneezing, runny or stuffy nose; or swollen or sore tongue.
This is not a complete list of side effects and others may occur. Tell your doctor about any unusual or bothersome side effect.
What other drugs will affect metronidazole?
Before taking this medication, tell your doctor if you are taking any of the following medicines:
Cimetidine (Tagamet); seizure medication such as phenytoin (Dilantin) or phenobarbital (Luminal, Solfoton); a blood thinner such as warfarin (Coumadin); lithium (Lithobid, Eskalith, others); or disulfiram (Antabuse).
This list is not a complete and there may be other drugs that can interact with metronidazole. Tell your doctor about all the prescription and over-the-counter medications you use. This includes vitamins, minerals, herbal products, and drugs prescribed by other doctors. Do not start using a new medication without telling your doctor. Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.From : Drug.com
Important about metronidazole
Take this medication for the entire length of time prescribed by your doctor. Your symptoms may get better before the infection is completely treated. Metronidazole will not treat a viral infection such as the common cold or flu. Do not drink alcohol while you are taking metronidazole and for at least 3 days after you stop taking it. You may have unpleasant side effects such as fast heartbeats, warmth or redness under your skin, tingly feeling, nausea, and vomiting.
Before taking metronidazole
Tell your doctor if you are pregnant or plan to become pregnant during treatment.
Before taking metronidazole, tell your doctor if you are allergic to any drugs, or if you have: Liver disease; a stomach or intestinal disease such as Crohn's disease; a blood cell disorder such as anemia (lack of red blood cells) or leukopenia (lack of white blood cells); epilepsy or other seizure disorder; or nerve disorders.
If you have any of these conditions, you may need a dose adjustment or special tests to safely take this medication. Metronidazole can pass into breast milk and may harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.
How should I take metronidazole?
Take this medication exactly as it was prescribed for you. Do not take the medication in larger amounts, or take it for longer than recommended by your doctor. Follow the directions on your prescription label. Take the extended-release form of metronidazole on an empty stomach, at least 1 hour before or 2 hours after eating a meal. Do not crush, chew, or break the extended-release tablet. Swallow the pill whole. It is specially made to release medicine slowly in the body. Breaking the pill would cause too much of the drug to be released at one time. Take this medication for the entire length of time prescribed by your doctor. Your symptoms may get better before the infection is completely treated. Metronidazole will not treat a viral infection such as the common cold or flu.
To be sure this medication is not causing harmful effects, your blood will need to be tested on a regular basis. Your liver function may also need to be tested. Do not miss any scheduled visits to your doctor.
This medication can cause you to have unusual results with certain medical tests. Tell any doctor who treats you that you are using metronidazole. Store metronidazole at room temperature away from moisture and heat.
What happens if I miss a dose?
Take the missed dose as soon as you remember. If it is almost time for your next dose, skip the missed dose and take the medicine at your next regularly scheduled time. Do not take extra medicine to make up the missed dose.
What happens if I overdose?
Seek emergency medical attention if you think you have used too much of this medicine.
Overdose symptoms may include nausea, vomiting, dizziness, loss of balance or coordination, numbness and tingling, or seizures (convulsions).
What should I avoid while taking metronidazole?
Do not drink alcohol while you are taking metronidazole and for at least 3 days after you stop taking it. You may have unpleasant side effects such as fast heartbeats, warmth or redness under your skin, tingly feeling, nausea, and vomiting.
Check the labels of any medicines or food products you use to make sure they do not contain alcohol. Antibiotic medicines can cause diarrhea, which may be a sign of a new infection. If you have diarrhea that is watery or has blood in it, call your doctor. Do not use any medicine to stop the diarrhea unless your doctor has told you to.
Metronidazole side effects
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Call your doctor at once if you have any of these serious side effects:
Seizures (convulsions); fever, chills, body aches, sore throat, flu symptoms; numbness or tingling in your hands or feet; white patches or sores inside your mouth or on your lips; pain or burning when you urinate; or diarrhea that is watery or bloody.
Less serious side effects may include:
Nausea, stomach pain, diarrhea; headache, dizziness, loss of balance; vaginal itching or discharge; dry mouth or unpleasant metallic taste; cough, sneezing, runny or stuffy nose; or swollen or sore tongue.
This is not a complete list of side effects and others may occur. Tell your doctor about any unusual or bothersome side effect.
What other drugs will affect metronidazole?
Before taking this medication, tell your doctor if you are taking any of the following medicines:
Cimetidine (Tagamet); seizure medication such as phenytoin (Dilantin) or phenobarbital (Luminal, Solfoton); a blood thinner such as warfarin (Coumadin); lithium (Lithobid, Eskalith, others); or disulfiram (Antabuse).
This list is not a complete and there may be other drugs that can interact with metronidazole. Tell your doctor about all the prescription and over-the-counter medications you use. This includes vitamins, minerals, herbal products, and drugs prescribed by other doctors. Do not start using a new medication without telling your doctor. Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.From : Drug.com
Calicivirus by DRUGS-HEALTH
Overview Feline calicivirus (pronounced cal-ee-chee, also known as FCV), a common viral disease that affects health cats , is characterized by upper respiratory symptoms, pneumonia, oral ulceration (sores in the mouth), and occasionally arthritis. It is a fairly mild flu-like condition and rarely causes serious complications.
Calicivirus is part of the feline upper respiratory infection (URI) complex, a group of viral and bacterial infections (e.g., FHV-1, chlamydiosis) that cause discharge from the eyes and nose. Calicivirus and feline rhinotracheitis virus account for 85% to 90% of all URIs in cats.
Incidence and Prevalence Calicivirus occurs worldwide and affects all breeds of cats. Vaccination has reduced the incidence of clinical disease, but it hasn't decreased the prevalence of the virus. The virus is spreading, even though fewer cats show symptoms.
Causes Numerous strains of feline calicivirus exist and different strains cause different symptoms (e.g., one particular strain can cause ulcers on the paws as well as in the mouth).
It usually affects the throat, and sometimes the lungs; it can also infect the intestines and has been isolated from feces. Calicivirus often occurs with another upper respiratory infection, such as feline herpes virus (FHV), rhinotracheitis virus, or chlamydiosis.
Transmission Calicivirus is spread through direct contact with the saliva, eye and nose discharges, and sometimes the feces, of an infected cat.
FCV is resistant to many disinfectants and can survive outside the cat's body for as long as 8 to 10 days, so it may be present in dishes, litter trays, and clothing, even after a thorough cleaning. Many cats remain contagious for years, even though they may not show signs of disease. Healthy (i.e., asymptomatic), contagious cats are known as latent carriers. Calicivirus is very common in kittens, multicat households, and pet adoption shelters. Outbreaks can occur in overcrowded, poorly ventilated, or unsanitary conditions; and where the cats are poorly fed, or stressed, either physically (e.g., extreme temperatures) or psychologically (e.g., introduction of a new cat). Until now nothing drug efective for theraphy calicivirus infection.
Calicivirus is part of the feline upper respiratory infection (URI) complex, a group of viral and bacterial infections (e.g., FHV-1, chlamydiosis) that cause discharge from the eyes and nose. Calicivirus and feline rhinotracheitis virus account for 85% to 90% of all URIs in cats.
Incidence and Prevalence Calicivirus occurs worldwide and affects all breeds of cats. Vaccination has reduced the incidence of clinical disease, but it hasn't decreased the prevalence of the virus. The virus is spreading, even though fewer cats show symptoms.
Causes Numerous strains of feline calicivirus exist and different strains cause different symptoms (e.g., one particular strain can cause ulcers on the paws as well as in the mouth).
It usually affects the throat, and sometimes the lungs; it can also infect the intestines and has been isolated from feces. Calicivirus often occurs with another upper respiratory infection, such as feline herpes virus (FHV), rhinotracheitis virus, or chlamydiosis.
Transmission Calicivirus is spread through direct contact with the saliva, eye and nose discharges, and sometimes the feces, of an infected cat.
FCV is resistant to many disinfectants and can survive outside the cat's body for as long as 8 to 10 days, so it may be present in dishes, litter trays, and clothing, even after a thorough cleaning. Many cats remain contagious for years, even though they may not show signs of disease. Healthy (i.e., asymptomatic), contagious cats are known as latent carriers. Calicivirus is very common in kittens, multicat households, and pet adoption shelters. Outbreaks can occur in overcrowded, poorly ventilated, or unsanitary conditions; and where the cats are poorly fed, or stressed, either physically (e.g., extreme temperatures) or psychologically (e.g., introduction of a new cat). Until now nothing drug efective for theraphy calicivirus infection.
27 April 2008
Effects and health issues of coccaine-DRUGS HEALTH
Cocaine is a potent central nervous system stimulant. Its effects can last from 20 minutes to several hours, depending upon the dosage of cocaine taken, purity, and method of administration.The initial signs of stimulation are hyperactivity, restlessness, increased blood pressure, increased heart rate and euphoria. The euphoria is sometimes followed by feelings of discomfort and depression and a craving to experience the drug again. Sexual interest and pleasure can be amplified. Side effects can include twitching, paranoia, and impotence, which usually increases with frequent usage.
With excessive dosage the drug can produce itching, tachycardia, hallucinations, and paranoid delusions. Overdoses cause tachyarrhythmias and a marked elevation of blood pressure. These can be life-threatening, especially if the user has existing cardiac problems. The LD50 of cocaine when administered to mice is 95.1 mg/kg. Toxicity results in seizures, followed by respiratory and circulatory depression of medullar origin. This may lead to death from respiratory failure, stroke, cerebral hemorrhage, or heart-failure. Cocaine is also highly pyrogenic, because the stimulation and increased muscular activity cause greater heat production. Heat loss is inhibited by the intense vasoconstriction. Cocaine-induced hyperthermia may cause muscle cell destruction and myoglobinuria resulting in renal failure. Emergency treatment often consists of administering a benzodiazepine sedation agent, such as diazepam (Valium) to decrease the elevated heart rate and blood pressure. Physical cooling (ice, cold blankets, etc...) and paracetamol(acetaminophen) may be used to treat hyperthermia, while specific treatments are then developed for any further complications. There is no officially approved specific antidote for cocaine overdose.
In cases where a patient is unable or unwilling to seek medical attention, cocaine overdoses resulting in mild-moderate tachycardia (i.e.: a resting pulse greater than 120 bpm), may be initially treated with 20 mg of orally administered diazepam or equivalent benzodiazepine (eg: 2mg lorazepam). Acetaminophen and physical cooling may likewise be used to reduce mild hyperthermia (<39>cardiac arrest or stroke, and requires immediate medical treatment. Cocaine's primary acute effect on brain chemistry is to raise the amount of dopamine and serotonin in the nucleus accumbens (the pleasure center in the brain); this effect ceases, due to metabolism of cocaine to inactive compounds and particularly due to the depletion of the transmitter resources (tachyphylaxis). This can be experienced acutely as feelings of depression, as a "crash" after the initial high. Further mechanisms occur in chronic cocaine use. The "crash" is accompanied with muscle spasms throughout the body, also known as the "jitters", muscle weakness, headaches, dizziness, and suicidal thoughts. Not all users will experience these, but most tend to experience some or all of these symptoms. Cocaine can cause coronary artery spasms which lead to a myocardial infarction. This effect can happen randomly to any user.
Chronic cocaine intake causes brain cells to adapt functionally to strong imbalances of transmitter levels in order to compensate extremes. Thus, receptors disappear from the cell surface or reappear on it, resulting more or less in an "off" or "working mode" respectively, or they change their susceptibility for binding partners (ligands) – mechanisms called down-/upregulation. Chronic cocaine use leads to a DATS upregulation. further contributing to depressed mood states. However, studies suggest cocaine abusers do not show normal age-related loss of striatal DAT sites, suggesting cocaine has neuroprotective properties for dopamine neurons. Physical withdrawal is not dangerous, and is in fact restorative. The lack of normal amounts of serotonin and dopamine in the brain is the cause of the dysphoria and depression felt after the initial high. The diagnostic criteria for cocaine withdrawal are characterized by a dysphoric mood, fatigue, unpleasant dreams, insomnia or hypersomnia, erectile dysfunction, increased appetite, psychomotor retardation or agitation, and anxiety.
Cocaine abuse also has multiple physical health consequences. It is associated with a lifetime risk of heart attack that is 6% higher than that of non-users. During the hour after cocaine is used, heart attack risk rises 24-fold. Side effects from chronic smoking of cocaine include hemoptysis, bronchospasm, pruritus, fever, diffuse alveolar infiltrates without effusions, pulmonary and systemic eosinophiliachest, pain, lung trauma, shortness of breath, sore throat, asthma, hoarse voice, dyspnea, and an aching, flu-like syndrome. Chronic intranasal usage can degrade the cartilage separating the nostrils (the septum nasi), leading eventually to its complete disappearance. Cocaine may also greatly increase this risk of developing rare autoimmune or connective tissue diseases such as lupus, Goodpasture's disease, vasculitis, glomerulonephritis, Stevens-Johnson syndrome and other diseases. It can also cause a wide array of kidney diseases and renal failure.[Cocaine abuse doubles both the risks of hemorrhagic and ischemic strokes.
So coccaine is very dangerous drugs for our health
With excessive dosage the drug can produce itching, tachycardia, hallucinations, and paranoid delusions. Overdoses cause tachyarrhythmias and a marked elevation of blood pressure. These can be life-threatening, especially if the user has existing cardiac problems. The LD50 of cocaine when administered to mice is 95.1 mg/kg. Toxicity results in seizures, followed by respiratory and circulatory depression of medullar origin. This may lead to death from respiratory failure, stroke, cerebral hemorrhage, or heart-failure. Cocaine is also highly pyrogenic, because the stimulation and increased muscular activity cause greater heat production. Heat loss is inhibited by the intense vasoconstriction. Cocaine-induced hyperthermia may cause muscle cell destruction and myoglobinuria resulting in renal failure. Emergency treatment often consists of administering a benzodiazepine sedation agent, such as diazepam (Valium) to decrease the elevated heart rate and blood pressure. Physical cooling (ice, cold blankets, etc...) and paracetamol(acetaminophen) may be used to treat hyperthermia, while specific treatments are then developed for any further complications. There is no officially approved specific antidote for cocaine overdose.
In cases where a patient is unable or unwilling to seek medical attention, cocaine overdoses resulting in mild-moderate tachycardia (i.e.: a resting pulse greater than 120 bpm), may be initially treated with 20 mg of orally administered diazepam or equivalent benzodiazepine (eg: 2mg lorazepam). Acetaminophen and physical cooling may likewise be used to reduce mild hyperthermia (<39>cardiac arrest or stroke, and requires immediate medical treatment. Cocaine's primary acute effect on brain chemistry is to raise the amount of dopamine and serotonin in the nucleus accumbens (the pleasure center in the brain); this effect ceases, due to metabolism of cocaine to inactive compounds and particularly due to the depletion of the transmitter resources (tachyphylaxis). This can be experienced acutely as feelings of depression, as a "crash" after the initial high. Further mechanisms occur in chronic cocaine use. The "crash" is accompanied with muscle spasms throughout the body, also known as the "jitters", muscle weakness, headaches, dizziness, and suicidal thoughts. Not all users will experience these, but most tend to experience some or all of these symptoms. Cocaine can cause coronary artery spasms which lead to a myocardial infarction. This effect can happen randomly to any user.
Chronic cocaine intake causes brain cells to adapt functionally to strong imbalances of transmitter levels in order to compensate extremes. Thus, receptors disappear from the cell surface or reappear on it, resulting more or less in an "off" or "working mode" respectively, or they change their susceptibility for binding partners (ligands) – mechanisms called down-/upregulation. Chronic cocaine use leads to a DATS upregulation. further contributing to depressed mood states. However, studies suggest cocaine abusers do not show normal age-related loss of striatal DAT sites, suggesting cocaine has neuroprotective properties for dopamine neurons. Physical withdrawal is not dangerous, and is in fact restorative. The lack of normal amounts of serotonin and dopamine in the brain is the cause of the dysphoria and depression felt after the initial high. The diagnostic criteria for cocaine withdrawal are characterized by a dysphoric mood, fatigue, unpleasant dreams, insomnia or hypersomnia, erectile dysfunction, increased appetite, psychomotor retardation or agitation, and anxiety.
Cocaine abuse also has multiple physical health consequences. It is associated with a lifetime risk of heart attack that is 6% higher than that of non-users. During the hour after cocaine is used, heart attack risk rises 24-fold. Side effects from chronic smoking of cocaine include hemoptysis, bronchospasm, pruritus, fever, diffuse alveolar infiltrates without effusions, pulmonary and systemic eosinophiliachest, pain, lung trauma, shortness of breath, sore throat, asthma, hoarse voice, dyspnea, and an aching, flu-like syndrome. Chronic intranasal usage can degrade the cartilage separating the nostrils (the septum nasi), leading eventually to its complete disappearance. Cocaine may also greatly increase this risk of developing rare autoimmune or connective tissue diseases such as lupus, Goodpasture's disease, vasculitis, glomerulonephritis, Stevens-Johnson syndrome and other diseases. It can also cause a wide array of kidney diseases and renal failure.[Cocaine abuse doubles both the risks of hemorrhagic and ischemic strokes.
So coccaine is very dangerous drugs for our health
Cortisol by DRUGS-HEALTH
Cortisol is the most potent glucocorticoid produced by the human adrenal. It is synthesized from cholesterol and its production is stimulated by pituitary adrenocorticotropic hormone (ACTH) which is regulated by corticotropin releasing factor (CRF). ACTH and CRF secretions are inhibited by high cortisol levels in a negative feedback loop. In plasma a majority of cortisol is bound with high affinity to corticosteroid binding globulin (CBG or transcotin). Cortisol acts through specific intracellular receptors and affects numerous physiologic systems including immune function, glucose counter regulation, vascular tone, and bone metabolism.
Cortisol production has an ACTH-dependent circadian rhythm with peak levels in the early morning and a nadir at night. The factor controlling this rhythm is not completely defined and can be disrupted by a number of physical and psychological conditions. ACTH and cortisol are secreted independent of circadian rhythm in response to physical and psychological stress.
Elevated cortisol levels and lack of diurnal variation have been identified with Cushing’s disease (ACTH hypersecretion). Elevated circulating cortisol levels have also been identified in patients with adrenal tumors. Low cortisol levels are found in primary adrenal insufficiency (e.g. adrenal hypoplasia, Addison’s disease) and in ACTH deficiency. Due to the normal circadian variation in cortisol levels, distinguishing normal from abnormally low cortisol levels can be difficult, therefore several daily collections are recommended.
Interpretation of ResultsCortisol levels in saliva reflect the active unbound compound. Cortisol is measured in ng/ml.
Salivary Cortisol Ranges for Women and Men
A.M. 1.0 - 8.0 P.M. 0.1 - 1.0
References1) Migeon CJ, Lanes RL: Adrenal cortex : hypo- and hyperfunction. IN Lifshitz F (ed): Pediatric Endocrinology. A Clinical Guide, 2nd edition. Marcel Dekker, Inc., NY 1990:333-3522) Hyams JS, Carey DE: Corticosteroids and growth. J Pediatr 1988;113:249-2543) Kreiger DT: Rhythms of ACTH and corticosteroid secretion in health and disease and their experimental modification. J Steroid Biochem 1975;6:785-7914) Stewart PM, Secl JR, Corrie J, Edwards CRW, Padfield PL: A rational approach for assessing the hypothalamo-pituitary-adrenal axis. Lancet 1988;5:1208-12105) Schlaghecke R, Komely E, Santen RT, Ridderskamp P: The effect of long-term glucocorticoid on pituitary-adrenal responses to exogenous corticotropin-releasing hormone. New Engl J Med 1992;326:226-2306) Aardal E, Holm AC: Cortisol in Saliva-Reference Ranges and Relation to Cortisol in Serum. Eur J Clin Chem Clin Biochem 1995;33:927-9237) Nicolson N, Storms C, Ponds R, Sulon J: Salivary Cortisol Levels and Stress Reactivity in Human Aging. J Gerontol 1997;52A:M68-M758) Greenspan FS, Stewler GJ (eds): Basic and Clinical Endocrinology. Appelton & Lange, Stamford, CT 1997
From Aeron Biotechnology Inc., all rights reserved
Toxicity of Clostridium tetani
C. tetani usually enters a host through a wound to the skin and then it replicates. Once an infection is established, C. tetani produces two exotoxins, tetanolysin and tetanospasmin. Eleven strains of C. tetani have been identified, which differ primarily in flagellar antigens and in its ability to produce tetanospasmin. The genes that produce toxin are encoded on a plasmid which is present in all toxigenic strains, and all strains that are capable of producing toxin produce identical toxins.
Tetanolysin serves no known function to C. tetani, and the reason the bacteria produce it is not known with certainty. Tetanospasmin is a neurotoxin and causes the clinical manifestations of tetanus. Tetanus toxin is generated in living bacteria, and is released when the bacteria lyses, such as during spore germination or during vegetative growth. A minimal amount of spore germination and vegetative cell growth are required for toxin production.
On the basis of weight, tetanospasmin is one of the most potent toxins known. The estimated minimum human lethal dose is 2.5 nanograms per kilogram of body weight, or 175 nanograms in a 70 kg (154 lb) human. The only toxins more lethal to humans are botulinum toxin, produced by close relative Clostridium botulinum and the exotoxin produced by Corynebacterium diphtheriae, the causative agent of diphtheria.
Tetanospasmin is a zinc-dependent metalloproteinase, that is similar in structure to botulinum toxin, but each toxin produces quite different effects. C. tetani synthesizes tetanospasmin as a single 150kDa polypeptide progenitor toxin, that is then cleaved by a protease into two fragments; fragment A (a 50kDa "light chain") and fragment B (a 100 kDa heavy chain) which remain connected via a disulfide bridge. Cleavage of the progenitor toxin into A and B fragments can also be induced artificially with trypsin.
Toxin Action
Tetanospasmin is distributed in the blood and lymphatic system of the host. The toxin acts at several sites within the central nervous system, including peripheral nerve terminals, the spinal cord, and brain, and within the sympathetic nervous system. The toxin is taken up into within the nerve axon and transported across synaptic junctions, until it reaches the central nervous system, where it is rapidly fixed to gangliosides at the presynaptic junctions of inhibitory motor nerve endings.
The clinical manifestations of tetanus are caused when tetanus toxin blocks inhibitory impulses, by interfering with the release of neurotransmitters, including glycine and gamma-aminobutyric acid. This leads to unopposed muscle contraction and spasm. Seizures may occur, and the autonomic nervous system may also be affected. Tetanospasmin appears to prevent the release of neurotransmitters by selectively cleaving a component of synaptic vesicles called synaptobrevin II.
It should be noted that the organism itself has no access to the nervous system, and yet tetanospasmin is directed toward the nervous system. The reason why this occurs, is still a subject of controversy. It's fairly known that toxins are by-products synthesized during bacterial growth, and their targets are determined by the presence or absence of specific receptors on human cells to which they can bind and exert their effect. This only explains why the tetanus toxin acts on the nervous system, but why it reaches a place to which the organism itself has no access may be an anomaly of nature.
From Wikipedia
Trachoma
Trachoma (Ancient Greek: "rough eye") is an infectious eye disease, and the leadingcause of the world's infectious blindness.
Trachoma is caused by the bacterium Chlamydia trachomatis and it is spread by direct contact with eye, nose, and throat secretions from affected individuals, or contact with fomites (inanimate objects), such as towels and/or washcloths, that have had similar contact with these secretions. Untreated, repeated trachoma infections result in a painful form of permanent blindness when the eyelids turn inward, causing the eyelashes to scratch the cornea. Children are the most susceptible to infection, but the blinding effects are often not felt until adulthood.
Blinding endemic trachoma occurs in areas with poor personal and family hygiene. Many factors are indirectly linked to the presence of trachoma including lack of water, absence of latrines or toilets, poverty in general, flies, close proximity to cattle, crowding and so forth.
Prevention
Although trachoma was eliminated from much of the developed world in the last century, this disease persists in many parts of the developing world particularly in communities without adequate access to water and sanitation. In many of these communities, women are three times more likely than men to be blinded by the disease.
Without intervention, trachoma keeps families shackled within a cycle of poverty, as the disease and its long-term effects are passed from one generation to the next.
National governments in collaboration with numerous non-profit organizations implement trachoma control programs using the WHO-recommended SAFE strategy, which includes:
Surgery to correct advanced stages of the disease;
Antibiotics to treat active infection, using Zithromax donated by Pfizer Inc through the International Trachoma Initiative;
Facial cleanliness to reduce disease transmission;
Environmental change to increase access to clean water and improved sanitation.
Surgery: For individuals with trichiasis, a bilamellar tarsal rotation procedure is warranted to direct the lashes away from the globe.Early intervention is beneficial as the rate of recurrence is higher in more advanced disease.
Antibiotic therapy: WHO Guidelines recommend that a region should receive community-based, mass antibiotic treatment when the prevalence of active trachoma among one to nine year-old children is greater than 10 percent. Subsequent annual treatment should be administered for three years, at which time the prevalence should be reassessed. Annual treatment should continue until the prevalence drops below five percent. At lower prevalences, antibiotic treatment should be family-based. Antibiotic selection: WHO recommends azithromycin (single oral dose of 20mg/kg) or topical tetracycline (one percent eye ointment twice a day for six weeks). Azithrtomycin is preferred because it is used as a single oral dose. InitiativeAzithromycin can be used in children from the age of six months and in pregnancy.
Facial cleanliness: Children with grossly visible nasal discharge, ocular discharge, or flies on their faces are at least twice as likely to have active trachoma as children with clean faces Intensive community-based health education programs to promote face-washing can significantly reduce the prevalence of active trachoma, especially intense trachoma (TI).
Environmental improvement: Modifications in water use, fly control, latrine use, health education and proximity to domesticated animals have all been proposed to reduce transmission of C. trachomatis. These changes pose numerous challenges for implementation. It seems likely that these environmental changes ultimately impact on the transmission of ocular infection by means of lack of facial cleanliness. Particular attention is required for environmental factors that limit clean faces.
Symptoms
The bacteria has an incubation period of 5 to 12 days, after which the affected individual experiences symptoms of conjunctivitis, or irritation similar to "pink eye." Blinding endemic trachoma results from multiple episodes of reinfection that maintains the intense inflammation in the conjunctiva. Without reinfection, the inflammation will gradually subside.
The World Health Organization recommends a simplified grading system for trachoma.
The Simplified WHO Grading System is summarized below:
• Trachomatous inflammation, follicular (TF) – Five or more follicles of >0.5mm on the upper tarsal conjunctiva
• Trachomatous inflammation, intense (TI) – Papillary hypertrophy and inflammatory thickening of the upper tarsal conjunctiva obscuring more than half the deep tarsal vessels
• Trachomatous trichiasis (TT) – At least one ingrown eyelash touching the globe, or evidence of epilation (eyelash removal)
• Corneal opacity (CO) – Corneal opacity blurring part of the pupil margin
Further symptoms include:
Eye discharge
Swollen eyelids
Trichiasis (turned-in eyelashes)
Swelling of lymph nodes in front of the ears
Corneal scarring
Further ear, nose and throat complications.
Prognosis
If not treated properly with oral antibiotics, the symptoms may escalate and cause blindness, which is the result of ulceration and consequent scarring of the cornea. Surgery may also be necessary to fix eyelid deformities.
Treatments for anemia
Anaemia is a body condition which blood insuffiency. anaemia because of disease attack, accident or because physiological condition. There are many different treatments for anemia and the treatment depends on severity and the cause. Anaemia is very often met, in light condition anaemia can be handled easily with the consumption medicinize or vitamin however in hard condition require to be conducted by a serious handling like blood transfusion.
Iron deficiency from nutritional causes is rare in non-menstruating adults. The diagnosis of iron deficiency mandates a search for potential sources of loss such as gastrointestinal bleeding from ulcers or colon cancer. Mild to moderate iron deficiency anemia is treated by iron supplementation with ferrous sulfate or ferrous gluconate. Vitamin C may aid in the body's ability to absorb iron.
Vitamin supplements given orally (folic acid) or subcutaneously (vitamin B-12) will replace specific deficiencies.
In anemia of chronic disease, anemia associated with chemotherapy, or anemia associated with renal disease, some clinicians prescribe recombinant erythropoietin, epoetin alfa, to stimulate red cell production.
In severe cases of anemia, or with ongoing blood loss, a blood transfusion may be necessary.
Blood transfusions for anemia
Doctors attempt to avoid blood transfusion in general, since multiple lines of evidence point to increased adverse patient clinical outcomes with more intensive transfusion strategies. The physiological principle that reduction of oxygen delivery associated with anemia leads to adverse clinical outcomes is balanced by the finding that transfusion does not necessarily mitigate these adverse clinical outcomes.
In severe, acute bleeding, transfusions of donated blood are often lifesaving. Improvements in battlefield casualty survival is attributable, at least in part, to the recent improvements in blood banking and transfusion techniques
Transfusion of the stable but anemic hospitalized patient has been the subject of numerous clinical trials, and transfusion is emerging as a deleterious intervention.
Four randomized controlled clinical trials have been conducted to evaluate aggressive versus conservative transfusion strategies in critically ill patients. All four of these studies failed to find a benefit with more aggressive transfusion strategies.
In addition, at least two retrospective studies have shown increases in adverse clinical outcomes with more aggressive transfusion strategies.
On the whole, these studies suggest that aggressive transfusions, at least for hospitalized patients, may at best not improve any clinical parameter, and at worst lead to adverse outcomes.
Prevention
Eat the nutritious food and according to body requirement
Take a rest the regular and enoughIf experiencing of haemorrahage hurt immediately discontinue haemorrahage
Iron deficiency from nutritional causes is rare in non-menstruating adults. The diagnosis of iron deficiency mandates a search for potential sources of loss such as gastrointestinal bleeding from ulcers or colon cancer. Mild to moderate iron deficiency anemia is treated by iron supplementation with ferrous sulfate or ferrous gluconate. Vitamin C may aid in the body's ability to absorb iron.
Vitamin supplements given orally (folic acid) or subcutaneously (vitamin B-12) will replace specific deficiencies.
In anemia of chronic disease, anemia associated with chemotherapy, or anemia associated with renal disease, some clinicians prescribe recombinant erythropoietin, epoetin alfa, to stimulate red cell production.
In severe cases of anemia, or with ongoing blood loss, a blood transfusion may be necessary.
Blood transfusions for anemia
Doctors attempt to avoid blood transfusion in general, since multiple lines of evidence point to increased adverse patient clinical outcomes with more intensive transfusion strategies. The physiological principle that reduction of oxygen delivery associated with anemia leads to adverse clinical outcomes is balanced by the finding that transfusion does not necessarily mitigate these adverse clinical outcomes.
In severe, acute bleeding, transfusions of donated blood are often lifesaving. Improvements in battlefield casualty survival is attributable, at least in part, to the recent improvements in blood banking and transfusion techniques
Transfusion of the stable but anemic hospitalized patient has been the subject of numerous clinical trials, and transfusion is emerging as a deleterious intervention.
Four randomized controlled clinical trials have been conducted to evaluate aggressive versus conservative transfusion strategies in critically ill patients. All four of these studies failed to find a benefit with more aggressive transfusion strategies.
In addition, at least two retrospective studies have shown increases in adverse clinical outcomes with more aggressive transfusion strategies.
On the whole, these studies suggest that aggressive transfusions, at least for hospitalized patients, may at best not improve any clinical parameter, and at worst lead to adverse outcomes.
Prevention
Eat the nutritious food and according to body requirement
Take a rest the regular and enoughIf experiencing of haemorrahage hurt immediately discontinue haemorrahage
Vertigo (medical)
Vertigo, a specific type of dizziness, is a major symptom of a balance disorder. It is the sensation of spinning or swaying while the body is stationary with respect to the earth or surroundings. There are two types of vertigo: subjective and objective. Subjective vertigo is when a person feels a false sensation of movement. Objective vertigo is when the surroundings will appear to move past a person's field of vision.
Causes
Vertigo is usually associated with a problem in the inner ear balance mechanisms (vestibular system), in the brain, or with the nerve connections between these two organs.
The most common cause of vertigo is benign paroxysmal positional vertigo, or BPPV. Vertigo can be a symptom of an inner ear infection. Vertigo can be a symptom of an underlying harmless cause, such as in BPPV or it can suggest more serious problems. These include drug toxicities (specifically gentamicin), strokes or tumors (though these are much less common than BPPV), syphilis
Vertigo can also be brought on suddenly through various actions or incidents, such as skull fractures or brain trauma, sudden changes of blood pressure, or as a symptom of motion sickness while sailing, riding amusement rides, airplanes or in a motor vehicle. Vertigo can also be caused by Carbon Monoxide poisoning. It is also one of the more common symptoms of superior canal dehiscence syndrome and Meniere's disease.Vertigo-like symptoms may also appear as paraneoplastic syndrome (PNS) in the form of opsoclonus myoclonus syndrome, a multi-faceted neurological disorder associated with many forms of incipient cancer lesions or virus.
Vertigo in context with the cervical spine
According to chiropractors, ligamental injuries of the upper cervical spine can result in head-neck-joint instabilities which can cause vertigo.[citation needed] In this view, instabilities of the head neck joint are affected by rupture or overstretching of the alar ligaments and/or capsule structures mostly caused by whiplash or similar biomechanical movements.
Symptoms during damaged alar ligaments besides vertigo often are dizziness; reduced vigilance, such as somnolence; seeing problems, such as seeing "stars", tunnel views or double contures. Some patients tell about unreal feelings that stands in correlation with depersonalization and attentual alterations
Medical doctors (MDs) do not endorse this explanation to vertigo due to a lack of any data to support it, from an anatomical or physiological standpoint. Often the patients who have an odyssey of medical consultations without any clear diagnosis and are sent to a psychiatrist because doctors think about depression or hypochondria. Standard imaging technologies such as CT Scan or MRI are not capable of finding instabilities without taking functional poses
Neurochemistry of vertigo
The neurochemistry of vertigo includes 6 primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-ocular reflex (VOR). Many others play more minor roles. Three neurotransmitters that work peripherally and centrally include glutamate, acetylcholine, and GABA. Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. GABA is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar Purkinje cells and the lateral vestibular nucleus, and the vertical VOR.
Three other neurotransmitters work centrally. Dopamine may accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. It is known that centrally acting antihistamines modulate the symptoms of motion sickness.The neurochemistry of emesis overlaps with the neurochemistry of motion sickness and vertigo. Acetylcholinc, histamine, and dopamine are excitatory neurotransmitters, working centrally on the control of emesis. GABA inhibits central emesis reflexes. Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.
Diagnostic
Tests of vestibular system (balance) function include electronystagmography (ENG), rotation tests, Caloric reflex test, and Computerized Dynamic Posturography (CDP).
Tests of auditory system (hearing) function include pure-tone audiometry, speech audiometry, acoustic-reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and auditory brainstem response test (ABR; also known as BER, BSER, or BAER). Other diagnostic tests include magnetic resonance imaging (MRI) and computerized axial tomography (CAT, or CT).
Treatment
Treatment is specific for underlying disorder of vertigo.Vestibular rehabilitation; anticholinergics; antihistamines; benzodiazepines; calcium channel antagonists, specifically Verapamil and Nimodipine; GABA modulators, specifically gabapentin and baclofen; Neurotransmitter reuptake inhibitors such as SSRI's, SNRI's and Tricyclics
Causes
Vertigo is usually associated with a problem in the inner ear balance mechanisms (vestibular system), in the brain, or with the nerve connections between these two organs.
The most common cause of vertigo is benign paroxysmal positional vertigo, or BPPV. Vertigo can be a symptom of an inner ear infection. Vertigo can be a symptom of an underlying harmless cause, such as in BPPV or it can suggest more serious problems. These include drug toxicities (specifically gentamicin), strokes or tumors (though these are much less common than BPPV), syphilis
Vertigo can also be brought on suddenly through various actions or incidents, such as skull fractures or brain trauma, sudden changes of blood pressure, or as a symptom of motion sickness while sailing, riding amusement rides, airplanes or in a motor vehicle. Vertigo can also be caused by Carbon Monoxide poisoning. It is also one of the more common symptoms of superior canal dehiscence syndrome and Meniere's disease.Vertigo-like symptoms may also appear as paraneoplastic syndrome (PNS) in the form of opsoclonus myoclonus syndrome, a multi-faceted neurological disorder associated with many forms of incipient cancer lesions or virus.
Vertigo in context with the cervical spine
According to chiropractors, ligamental injuries of the upper cervical spine can result in head-neck-joint instabilities which can cause vertigo.[citation needed] In this view, instabilities of the head neck joint are affected by rupture or overstretching of the alar ligaments and/or capsule structures mostly caused by whiplash or similar biomechanical movements.
Symptoms during damaged alar ligaments besides vertigo often are dizziness; reduced vigilance, such as somnolence; seeing problems, such as seeing "stars", tunnel views or double contures. Some patients tell about unreal feelings that stands in correlation with depersonalization and attentual alterations
Medical doctors (MDs) do not endorse this explanation to vertigo due to a lack of any data to support it, from an anatomical or physiological standpoint. Often the patients who have an odyssey of medical consultations without any clear diagnosis and are sent to a psychiatrist because doctors think about depression or hypochondria. Standard imaging technologies such as CT Scan or MRI are not capable of finding instabilities without taking functional poses
Neurochemistry of vertigo
The neurochemistry of vertigo includes 6 primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-ocular reflex (VOR). Many others play more minor roles. Three neurotransmitters that work peripherally and centrally include glutamate, acetylcholine, and GABA. Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. GABA is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar Purkinje cells and the lateral vestibular nucleus, and the vertical VOR.
Three other neurotransmitters work centrally. Dopamine may accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. It is known that centrally acting antihistamines modulate the symptoms of motion sickness.The neurochemistry of emesis overlaps with the neurochemistry of motion sickness and vertigo. Acetylcholinc, histamine, and dopamine are excitatory neurotransmitters, working centrally on the control of emesis. GABA inhibits central emesis reflexes. Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.
Diagnostic
Tests of vestibular system (balance) function include electronystagmography (ENG), rotation tests, Caloric reflex test, and Computerized Dynamic Posturography (CDP).
Tests of auditory system (hearing) function include pure-tone audiometry, speech audiometry, acoustic-reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and auditory brainstem response test (ABR; also known as BER, BSER, or BAER). Other diagnostic tests include magnetic resonance imaging (MRI) and computerized axial tomography (CAT, or CT).
Treatment
Treatment is specific for underlying disorder of vertigo.Vestibular rehabilitation; anticholinergics; antihistamines; benzodiazepines; calcium channel antagonists, specifically Verapamil and Nimodipine; GABA modulators, specifically gabapentin and baclofen; Neurotransmitter reuptake inhibitors such as SSRI's, SNRI's and Tricyclics
Viagra / Sildenafil
Systematic (IUPAC) name
1-[4-ethoxy-3-(6,7-dihydro-1-methyl-7-oxo-3-propyl-1H-pyrazolo[4,3-d]pyrimidin-5-yl) phenylsulfonyl]-4-methylpiperazine citrate
Formula C22H30N6O4S
Mol. mass base: 474.6g/mol
Bioavailability 40%
Metabolism Hepatic
Half life 3-4hRoutesOral
Sildenafil citrate, sold under the names Viagra, Revatio and under various other names, is a drug used to treat male erectile dysfunction (impotence) and pulmonary arterial hypertension (PAH), developed by the pharmaceutical company Pfizer. Its primary competitors on the market are tadalafil (Cialis), and vardenafil (Levitra)..
Mechanism of action
Part of the physiological process of erection involves the parasympathetic nervous system causing the release of nitric oxide (NO) in the corpus cavernosum of the penis. NO binds to the receptors of the enzyme guanylate cyclase which results in increased levels of cyclic guanosine monophosphate (cGMP), leading to smooth muscle relaxation (vasodilation) of the intimal cushions of the helicine arteries, resulting in increased inflow of blood and an erection.
Sildenafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum. The molecular structure of sildenafil is similar to that of cGMP and acts as a competitive binding agent of PDE5 in the corpus cavernosum, resulting in more cGMP and better erections. Without sexual stimulation, and therefore lack of activation of the NO/cGMP system, sildenafil should not cause an erection. Other drugs that operate by the same mechanism include tadalafil (Cialis) and vardenafil (Levitra).
Sildenafil is metabolised by hepatic enzymes and excreted by both the liver and kidneys. If taken with a high-fat meal, there may be a delay in absorption of sildenafil and the peak effect might be reduced slightly as the plasma concentration will be lowered.
Dosage and price
As with all prescription drugs, proper dosage is at the discretion of a licensed medical doctor. The dose of sildenafil for erectile dysfunction is 25 mg to 100 mg taken not more than once per day between 30 minutes and 4 hours prior to sexual intercourse.
It is usually recommended to start with a dosage of 50 mg and then lower or raise the dosage as appropriate. The drug is sold in three dosages (25, 50, and 100 mg), all three costing about US$10 per pill. Name-brand Viagra sildenafil is not scored and a fairly hard coating makes it more difficult to accurately cut the pills in half, even with a pill cutter. The dosage for pulmonary arterial hypertension (Revatio) is one 20 mg tablet three times a day. Viagra pills are blue and diamond-shaped with the words "Pfizer" engraved on one side, and "VGR xx" (where xx stands for "25", "50" or "100", the dose of that pill in milligrams) engraved on the other. Words are not printed on the pills. Revatio pills, which are used for PAH, are white, round, film-coated tablets imprinted with "RVT 20" on one side and "Pfizer" on the other.
Contraindications
Contraindications include:
· When taking nitric oxide donors, organic nitrites and nitrates, such as glyceryl trinitrate (nitroglycerin), sodium nitroprusside, amyl nitrite ("poppers")[6]
· In men for whom sexual intercourse is inadvisable due to cardiovascular risk factors
· Severe hepatic impairment (decreased liver function)
· Severe impairment in renal function
· Hypotension (low blood pressure)
· Recent stroke or heart attack
· Hereditary degenerative retinal disorders (including genetic disorders of retinal phosphodiesterases)
Chemical synthesis
The preparation steps for synthesis of Viagra (sildenafil citrate) are as follows:
1. Methylation of 3-propylpyrazole-5-carboxylic acid ethyl ester with hot dimethyl sulfate.
2. Hydrolysis with aqueous NaOH to free acid.
3. Nitration with oleum/fuming nitric acid.
4. Carboxamide formation with refluxing thionyl chloride/NH4OH.
5. Reduction of nitro group to amino.
6. Acylation with 2-ethoxybenzoyl chloride.
7. Cyclization.
8. Sulfonation to the chlorosulfonyl derivative.
9. Condensation with 1-methylpiperazine.
24 April 2008
Herb for the Child
Herb usage have become the alternative in medication and disease prevention propose the increasing of chemical drug price and the increasing of society enthusiasm to natural substance use from nature in life all day long In this case ordinary herb accumulator weared as medication complement.
Herb own the excess because do not or only a few once risk side effects generated. But that way in its use especially for the medication of children needed by extra attention in order not to be happened by a bad effect in the case of this is needed a role and also parent.
Several things which require to be paid attention to in herb usage for children :
Searching information by asking to herb expert which have experienced or doctor in order not to there is mistake in usage or herb election
Avoid existing of poisonous or toxic content
Labouring don't too bitter or if perforced hence bitter herb enhance the honey or palm sugar sufficiently
Give the dose ½ adult dose
Accustoming hence substance to once just just processing
Beware when make of it and clean ahead substance [in] water emit a stream of 10-15 minute and pan don't made from alumunium
If there [is] allergic symptom better [is] immediately discontinued and consultancy craftily herb or doctor
Follow the example of the ingredient :
For cough and have a cold
½ grasp the dry saga (traditional name) + 1 dry fennel teaspoon braise in 3 glass irrigate [is] till remained [by] 2 just just glass. Drinking warm moment 2x one day before and hereafter eat the
Herb own the excess because do not or only a few once risk side effects generated. But that way in its use especially for the medication of children needed by extra attention in order not to be happened by a bad effect in the case of this is needed a role and also parent.
Several things which require to be paid attention to in herb usage for children :
Searching information by asking to herb expert which have experienced or doctor in order not to there is mistake in usage or herb election
Avoid existing of poisonous or toxic content
Labouring don't too bitter or if perforced hence bitter herb enhance the honey or palm sugar sufficiently
Give the dose ½ adult dose
Accustoming hence substance to once just just processing
Beware when make of it and clean ahead substance [in] water emit a stream of 10-15 minute and pan don't made from alumunium
If there [is] allergic symptom better [is] immediately discontinued and consultancy craftily herb or doctor
Follow the example of the ingredient :
For cough and have a cold
½ grasp the dry saga (traditional name) + 1 dry fennel teaspoon braise in 3 glass irrigate [is] till remained [by] 2 just just glass. Drinking warm moment 2x one day before and hereafter eat the
Gentamicin
Systematic (IUPAC) name
2-[4,6-diamino-3- [3-amino-6-(1-methylaminoethyl) tetrahydropyran-2-yl] oxy-2-hydroxy- cyclohexoxy]-5-methyl- 4-methylamino-tetrahydropyran-3,5-dio
Excretion renal
Half life 2 hours
Routes IV/IM
Protein binding 0-10%
Bioavailability limited oral bioavailability
FormulaC21H43N5O7
Mol. mass 477.596 g/mol
Molecular model showing how Gentamicin binds to bacterial DNA
Gentamicin is an aminoglycoside antibiotic, used to treat many types of bacterial infections, particularly those caused by Gram-negative bacteria. However, gentamicin is not used for Neisseria gonorrhoeae, Neisseria meningitidis or Legionella pneumophila bacterial infections.
It is synthesized by Micromonospora, a genus of Gram-positive bacteria widely present in the environment (water and soil). To highlight their specific biological origins, gentamicin and other related antibiotics produced by this genus (verdamicin, mutamicin, sisomicin, netilmicin, retymicin) have generally their spellings ending in ~micin and not in ~mycin. Gentamicin is a bactericidal antibiotic that works by binding the 50S subunit of the bacterial ribosome, interrupting protein synthesis.
Like all aminoglycosides, when gentamicin is given orally, it is not systemically active. This is because it is not absorbed to any appreciable extent from the small intestine. It appears to be completely eliminated unchanged in the urine. Urine must be collected for many days to recover all of a given dose because the drug binds avidly to certain tissues. It is administered intravenously, intramuscularly or topically to treat infections.
E. coli has shown some resistance to gentamicin, despite being Gram-negative. Gentamicin is one of the few heat-stable antibiotics that remain active even after autoclaving, which makes it particularly useful in the preparation of certain microbiological growth media.Treatment of susceptible bacterial infections, normally Gram-negative bacteria including Pseudomonas, Proteus, Serratia, and Gram-positive Staphylococcus.
Side effects
All aminoglycosides are toxic to the sensory cells of the ear, but they vary greatly in their relative effects on hearing versus balance. Gentamicin is a vestibulotoxin, and can cause permanent loss of equilibrioception, caused by damage to the vestibular apparatus of the inner ear if taken at high doses or for prolonged periods of time. Gentamicin has on occasion impaired or even wholly destroyed hearing. In most instances, the affected individual has undergone treatment for 2 weeks or more. A small number of affected individuals have a normally harmless mutation in their mitochondrial RNA, that allows the gentamicin to affect their cells. The cells of the ear are particularly sensitive to this. Gentamicin is sometimes used intentionally for this purpose in severe Ménière's disease, to disable the vestibular apparatus.
Gentamicin can also be highly nephrotoxic, particularly if multiple doses accumulate over a course of treatment. For this reason gentamicin is usually dosed by body weight. Various formulae exist for calculating gentamicin dosage. Also trough and peak serum levels of gentamicin are monitored during treatment, generally before and after the third dose is infused. Gentamicin, like other aminoglycosides, causes nephrotoxicity by inhibiting protein synthesis in renal cells. This mechanism specifically causes necrosis of cells in the proximal tubule, resulting in acute tubular necrosis which can lead to acute renal failure.
From Wikipedia, the free encyclopedia
2-[4,6-diamino-3- [3-amino-6-(1-methylaminoethyl) tetrahydropyran-2-yl] oxy-2-hydroxy- cyclohexoxy]-5-methyl- 4-methylamino-tetrahydropyran-3,5-dio
Excretion renal
Half life 2 hours
Routes IV/IM
Protein binding 0-10%
Bioavailability limited oral bioavailability
FormulaC21H43N5O7
Mol. mass 477.596 g/mol
Molecular model showing how Gentamicin binds to bacterial DNA
Gentamicin is an aminoglycoside antibiotic, used to treat many types of bacterial infections, particularly those caused by Gram-negative bacteria. However, gentamicin is not used for Neisseria gonorrhoeae, Neisseria meningitidis or Legionella pneumophila bacterial infections.
It is synthesized by Micromonospora, a genus of Gram-positive bacteria widely present in the environment (water and soil). To highlight their specific biological origins, gentamicin and other related antibiotics produced by this genus (verdamicin, mutamicin, sisomicin, netilmicin, retymicin) have generally their spellings ending in ~micin and not in ~mycin. Gentamicin is a bactericidal antibiotic that works by binding the 50S subunit of the bacterial ribosome, interrupting protein synthesis.
Like all aminoglycosides, when gentamicin is given orally, it is not systemically active. This is because it is not absorbed to any appreciable extent from the small intestine. It appears to be completely eliminated unchanged in the urine. Urine must be collected for many days to recover all of a given dose because the drug binds avidly to certain tissues. It is administered intravenously, intramuscularly or topically to treat infections.
E. coli has shown some resistance to gentamicin, despite being Gram-negative. Gentamicin is one of the few heat-stable antibiotics that remain active even after autoclaving, which makes it particularly useful in the preparation of certain microbiological growth media.Treatment of susceptible bacterial infections, normally Gram-negative bacteria including Pseudomonas, Proteus, Serratia, and Gram-positive Staphylococcus.
Side effects
All aminoglycosides are toxic to the sensory cells of the ear, but they vary greatly in their relative effects on hearing versus balance. Gentamicin is a vestibulotoxin, and can cause permanent loss of equilibrioception, caused by damage to the vestibular apparatus of the inner ear if taken at high doses or for prolonged periods of time. Gentamicin has on occasion impaired or even wholly destroyed hearing. In most instances, the affected individual has undergone treatment for 2 weeks or more. A small number of affected individuals have a normally harmless mutation in their mitochondrial RNA, that allows the gentamicin to affect their cells. The cells of the ear are particularly sensitive to this. Gentamicin is sometimes used intentionally for this purpose in severe Ménière's disease, to disable the vestibular apparatus.
Gentamicin can also be highly nephrotoxic, particularly if multiple doses accumulate over a course of treatment. For this reason gentamicin is usually dosed by body weight. Various formulae exist for calculating gentamicin dosage. Also trough and peak serum levels of gentamicin are monitored during treatment, generally before and after the third dose is infused. Gentamicin, like other aminoglycosides, causes nephrotoxicity by inhibiting protein synthesis in renal cells. This mechanism specifically causes necrosis of cells in the proximal tubule, resulting in acute tubular necrosis which can lead to acute renal failure.
From Wikipedia, the free encyclopedia
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