Health Hazard Information of Catechol

Chemical and physical properties

The chemical formula for catechol is C6H6O2, and its molecular weight is 110.11 g/mol.Catechol occurs as colorless tablets or monoclinic crystals that discolor in air and are soluble in water. It has a faint, phenolic odor; the odor threshold has not been established. The vapor pressure for catechol is 0.03 mm Hg at 20 degree, its log octanol/water partition coefficient (log Kow) is 0.88, and the CAS NO is 120-80-9.

Uses and applications

Synthetic catechol is an organic aromatic compound, appearing under the form of colourless solid flakes which darken upon exposure to air and light. It is mainly used as an intermediate for the synthesis of pharmaceuticals, agrochemicals and in formulation.

It is a precursor to various flavourings such as vanillin or eugenol (synthetic “vanilla” aroma and flavour), used in food industry, perfumery, home and personal care products. This chemical route of vanillin synthesis is far more environmentally friendly than the o-nitrochlorobenzene route. The production is performed using conventional closed vessels. The process is widely acknowledged as the Best Available Technology in terms of reduced water and energy consumption.

Health Hazard Information

Acute Effects:
Skin contact causes eczematous dermatitis in humans.In humans, absorption through the skin results in an illness resembling that induced by phenol, except convulsions are more pronounced.

Large doses of catechol can cause depression of the CNS and a prolonged rise of blood pressure in animals. The rise of blood pressure appears to be due to peripheral vasoconstriction.Due to the lack of information regarding the duration of exposure in the above studies, it is not clear whether these health effects were observed following acute or chronic exposure.Acute animal tests in rats, mice, guinea pigs, and rabbits have demonstrated catechol to have high acute toxicity by oral or dermal exposure.

Chronic Effects (Noncancer):
No information is available on the chronic effects of catechol in humans or animals.EPA has not established a Reference Concentration (RfC) or a Reference Dose (RfD) for catechol.

Reproductive/Developmental Effects:
No information is available on the reproductive or developmental effects of catechol in humans or animals.

Cancer Risk:
No information is available on the carcinogenic effects of catechol in humans.In orally exposed rats, adenocarcinomas in the glandular stomach were reported.

Catechol increased the carcinogenic effects of benzo[a]pyrene on the skin in mice when applied together dermally. No increase in malignant tumors was observed in orally exposed mice. EPA has not classified catechol with respect to potential carcinogenicity.IARC has classified catechol as a Group 2B, possibly carcinogenic to humans.

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Important warning about Mifepristone

Mifepristone is a synthetic steroid compound used as a pharmaceutical. It is a progesterone receptor antagonist used as an abortifacient in the first months of pregnancy, and in smaller doses as an emergency contraceptive. Mifepristone is also a powerful glucocorticoid receptor antagonist, and has occasionally been used in refractory Cushing’s Syndrome .

Mifepristone(CAS NO:84371-65-3) is used, together with another medication called misoprostol, to end an early pregnancy (within 49 days of the start of a woman’s last menstrual period). Since its approval in September 2000, the Food and Drug Administration has received reports of serious adverse events, including several deaths, in the United States following medical abortion with mifepristone and misoprostol. Each time FDA receives a report of a serious adverse event or death after medical abortion with these drugs, the agency carefully analyzes the available scientific information to determine whether or not the serious adverse event or death is related to the use of the drugs.

As previously reported by the agency, several of the women who died in the United States died from sepsis (severe illness caused by infection of the bloodstream) after medical abortion with mifepristone and misoprostol. Sepsis is a known risk related to any type of abortion. Most of these women were infected with the same type of bacteria, known as Clostridium sordellii. The symptoms in these cases of infection were not the usual symptoms of sepsis. We do not know whether using mifepristone and misoprostol caused these deaths. Here are some important warnings about using Mifepristone, it may give you some help to use it safety.

Serious or life-threatening vaginal bleeding may occur when a pregnancy is ended by miscarriage or by medical or surgical abortion. It is not known if taking mifepristone increases the risk that you will experience very heavy bleeding. Tell your doctor if you have or have ever had bleeding problems, an ectopic pregnancy (‘tubal pregnancy’ or pregnancy outside the uterus), anemia (less than normal number of red blood cells), or if you are taking anticoagulants (‘blood thinners’) such as warfarin (Coumadin), heparin, or aspirin. If you experience very heavy vaginal bleeding, such as soaking through two thick full-size sanitary pads every hour for two continuous hours, call your doctor immediately or seek emergency medical care.

Serious or life threatening infections may occur when a pregnancy is ended by miscarriage or by medical or surgical abortion. A small number of patients died due to infections that they developed after they used mifepristone and misoprostol to end their pregnancies. Some of these patients had used misoprostol vaginally; vaginal use of oral misoprostol tablets has not been approved by the Food and Drug Administration (FDA). It is not known if mifepristone and/or misoprostol taken vaginally or by mouth caused these infections or deaths.

If you develop a serious infection, you may not have many symptoms and your symptoms may not be very severe. You should call your doctor immediately if you experience any of the following symptoms: fever greater than 100.4 °F that lasts for more than 4 hours, severe pain or tenderness in the area below the waist, chills, fast heartbeat, or fainting.

You should also call your doctor immediately if you have general symptoms of illness such as weakness, nausea, vomiting, diarrhea, or feeling sick more than 24 hours after taking this medicine even if you do not have a fever or pain in the area below your waist.

Your doctor will give you the manufacturer’s patient information sheet (Medication Guide) to read before you begin treatment with mifepristone. You will also need to sign a patient agreement before taking this medicine. Tell your doctor if you have questions about treatment with this medicine or if you cannot follow the guidelines in the patient agreement.

Talk to your doctor and decide whom to call and what to do in case of an emergency after taking mifepristone. Tell your doctor if you do not think that you will be able to follow this plan or to get medical treatment quickly in an emergency during the first two weeks after you take mifepristone. Take your medication guide with you if you visit an emergency room or seek emergency medical care so that the doctors who treat you will understand that you are undergoing a medical abortion.

Keep all appointments with your doctor. These appointments are necessary to be sure that your pregnancy has ended and that you have not developed serious complications of medical abortion.Talk to your doctor about the risks of taking mifepristone.

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The future of Temozolomide

Temozolomide is a white to light tan/light pink powder with a molecular formula of C6H6N6O2 and a molecular weight of 194.15. The molecule is stable at acidic pH ( < 5) and labile at pH > 7; hence TEMODAR can be administered orally and intravenously. The prodrug, temozolomide, is rapidly hydrolyzed to the active 5-(3-methyltriazen-1-yl) imidazole-4-carboxamide (MTIC) at neutral and alkaline pH values, with hydrolysis taking place even faster at alkaline pH.

Temozolomide(CAS NO:85622-93-1) is now used worldwide to treat the most common adult brain tumour, called glioblastoma, as well as some other types. In combination with radiotherapy, it has become the international standard-of-care for thousands of people with this type of cancer.

Laboratory studies and clinical trials are investigating whether it might be possible to further increase the anticancer potency of temozolomide by combining it with other pharmacologic agents. For example, clinical trials have indicated that the addition of chloroquine might be beneficial for the treatment of glioma patients.

In laboratory studies, it was found that temozolomide killed brain tumor cells more efficiently when epigallocatechin gallate (EGCG), a component of green tea, was added; however, the efficacy of this effect has not yet been confirmed in brain tumor patients. More recently, use of the novel oxygen diffusion-enhancing compound trans sodium crocetinate (TSC) when combined with this medicine and radiation therapy has been investigated in preclinical studies and a clinical trial is currently underway.

Cancer Research UK scientists led the development of temozolomide. From early pioneering lab work, to the discovery, development and first clinical trials of the drug in people with cancer, our researchers were involved every step of way.

The undisputed ‘father’ of temozolomide is Malcolm Stevens, now Emeritus Professor at the University of Nottingham.We spoke to him to find out more about this medicine and its future fate.

Worldwide sales of temozolomide have now reached 1 billion dollars. Because of our partnership with Schering-Plough, we receive a royalty on this. The money is ploughed straight back into our research, funding new work into the prevention, diagnosis and treatment of cancer.

But the story of temozolomide doesn’t end here. The drug continues to benefit more and more people each year—people like Parminder, who was diagnosed with a brain tumour in 2011, when she was just 28. She had surgery and radiotherapy, as well as two courses of this medicine, and it looks like her tumour is gone for now. As well as being back on her feet (last year she ran Race For Life to support our research) she’s now back at work as an advertising sales executive.

“Personally, I found it was a hard course of treatment to have, but I am glad to have got through it”, she says. “I am so grateful for the treatment that I had and I think it is fantastic how organisations like Cancer Research UK are working on developing these treatments for the future.”

For now Parminder is doing well, and we’re all keeping our fingers crossed that things stay that way. And for many thousands of people around the world going through treatment for brain tumours, temozolomide is playing a vital role in the treatment that is helping to control their disease, giving them precious months, years and even decades more with their families.

Our scientists are now testing whether the drug can be used for other types of cancer, and continue to refine how it’s used to treat patients through clinical trials. This includes OPARATIC, an important trial testing temozolomide in combination with new drugs called PARP inhibitors for glioblastoma. This trial, and others like it, could bring important benefits to many more people in future.

The discovery and development of temozolomide would not have been possible without the support of the public and with your continued support, we’ll be able to carry on developing the life-saving treatments of tomorrow.

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History of Pearl millet

Pearl millet is the most widely grown type of millet. It has been grown in Africa and the Indian subcontinent since prehistoric times. The center of diversity, and suggested area of domestication, for the crop is in the Sahel zone of West Africa.

Recent archaeobotanical research has confirmed the presence of domesticated pearl millet on the Sahel zone of northern Mali between 2500 and 2000 BC. Cultivation subsequently spread and moved overseas to India. The earliest archaeological records in India date to around 2000 BC, and it spread rapidly through India reaching South India by 1500 BC, based on evidence from the site of Hallur. Cultivation also spread throughout eastern and southern Africa. Records exist for cultivation of pearl millet in the United States in the 1850s, and the crop was introduced into Brazil in the 1960s.

Pearl millet is well adapted to growing areas characterized by drought, low soil fertility, and high temperature. It performs well in soils with high salinity or low pH. Because of its tolerance to difficult growing conditions, it can be grown in areas where other cereal crops, such as maize or wheat, would not survive. Today pearl millet is grown on over 260,000 km2 worldwide. It accounts for approximately 50% of the total world production of millets.

Pearl millet is today an enormously important staple cereal of both sub-saharan Africa and parts of India; and an important forage crop in the Americas. Archaeological evidence suggests that pearl millet was first domesticated in the grasslands and park lands at the edge of the savanna-sahel desert of west Africa ca 2500 BC, and spread rapidly out from there.

Researchers believe that the development and spread of millet farming was spurred by the increasing desiccation of the Sahara Desert after 3000 BC. Millet domestication followed the domestication of cattle in Africa by at least 1500 years, and it is hypothesized that that is because mobile pastoralism was better suited to the region prior to the onset of the dessication.

By the second millennium BC, pearl millet was the primary food plant in Mali, Mauritania, Ghana, Burkina Faso and Cameroon. Pearl millet appears in south Asia no later than 2300 BC, with early evidence at Gujarat, Koethe, Babor Kot, and Surkotada in India.

The earliest evidence for pearl millet domestication comes from the Lower Tilemsi Valley in eastern Mali, specifically at the sites of Karkarichinkat Sud and Karkarichinkat Nord. Dates for dependence on the grain (not necessarily domesticated) at these sites begin ca 5500-4500 BP (or ~3500-2500 BC). Stable isotope analysis of human remains from these sites also support reliance on millet at this date. Enzyme similarity of modern pearl millet supports this as well, pointing to western Africa, with a domestication center between northeast Mali to Lake Chad.

Birimi in northern Ghana contained domesticated millet grains direct-dated to 3490 BP (1787-1744 cal BC). Ceramics at Dhar Tichitt in southwestern Maritania contained impressions of domesticated pearl millet dated to 3800 BP.

In addition to the presence of millet seeds, rachises, and bristle fragments within the assemblages at the Karakarichinkat sites, archaeological evidence for the presence of domesticated pearl millet includes pottery tempered with millet chaff.

Dates supporting the domestication of pearl millet at Karkarichinkat included Accelerator(DM) Mass Spectrometery (AMS) radiocarbon dates on associated charcoal including one firmly identified grain of domesticated pearl millet, as well as optically stimulated luminescence (OSL) dates on potsherds and soil sediments. Together, these put the domestication of pearl millet at approximately 2500 BC.

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How to take Diosmin?

Diosmin is a type of plant chemical found mainly in citrus fruits. People use diosmin to make medicine. It is a semisynthetic drug (modified hesperidin), a member of the flavonoid family. It is an oral phlebotropic drug used in the treatment of venous disease, i.e., chronic venous insufficiency (CVI) and hemorrhoidal disease (HD), in acute or chronic hemorrhoids, in place of rubber-band ligation, in combination with fiber supplement, or as an adjuvant therapy to hemorrhoidectomy, in order to reduce secondary bleeding. To control internal symptoms of hemorrhoids (piles), it is used with hesperidin.

Diosmin(CAS NO: 520-27-4) is used for treating various disorders of blood vessels including hemorrhoids, varicose veins, poor circulation in the legs (venous stasis), and bleeding (hemorrhage) in the eye or gums. It is also used to treat swelling of the arms (lymphedema) following breast cancer surgery, and to protect against liver toxicity. It is often taken in combination with hesperidin, another plant chemical.

Diosmin prolongs the vasoconstrictor effect of norepinephrine on the vein wall, increasing venous tone, and therefore reducing venous capacitance, distensibility, and stasis. This increases the venous return and reduces venous hyperpressure present in patients suffering from CVI.

Diosmin improves lymphatic drainage by increasing the frequency and intensity of lymphatic contractions, and by increasing the total number of functional lymphatic capillaries. Furthermore, this medicine with hesperidine decreases the diameter of lymphatic capillaries and the intralymphatic pressure.

At the microcirculation level, diosmin reduces capillary hyperpermeability and increases capillary resistance by protecting the microcirculation from damaging processes. It reduces the expression of endothelial adhesion molecules (ICAM1, VCAM1), and inhibits the adhesion, migration, and activation of leukocytes at the capillary level. This leads to a reduction in the release of inflammatory mediators, principally oxygen free radicals and prostaglandins (PGE2, PGF2a).

Diosmin is often taken in combination with hesperidin.The following doses have been studied in scientific research:

By mouth:

For the treatment of internal hemorrhoids: 1350 mg of diosmin plus 150 mg of hesperidin twice daily for 4 days followed by 900 mg of this medicine and 100 mg of hesperidin twice daily for 3 days. Some researchers also try 600 mg of this medicine three times daily for 4 days, followed by 300 mg twice daily for 10 days, in combination with 11 grams of psyllium daily. However, this lower diosmin dose does not seem to be as effective.

For prevention of relapse internal hemorrhoids: 450 mg of this medicine plus 50 mg of hesperidin twice daily for 3 months of therapy.

For the treatment of leg wounds due to bloodflow problems (venous stasis ulcers): the combination of 900 mg of this medicine and 100 mg of hesperidin daily has been used for up to 2 months.

Diosmin is safe for most people when used short-term for up to three months. It can cause some side effects such as stomach and abdominal pain, diarrhea, and headache. Do not take it for more than three months without medical supervision.

Here are some Special Precautions & Warnings about Diosmin, you should be careful: Pregnancy and breast-feeding: Not enough is known about the use of diosmin during pregnancy and breast-feeding. Stay on the safe side and avoid use.

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Learning about Alendronate sodium

Alendronate sodium is a bisphosphonate that acts as a specific inhibitor of osteoclastmediated bone resorption. Bisphosphonates are synthetic analogs of pyrophosphate that bind to the hydroxyapatite found in bone.

Alendronate sodium is chemically described as (4-amino-1-hydroxybutylidene) bisphosphonic acid monosodium salt trihydrate. The empirical formula of alendronate sodium is C4H12NNaO7P2•3H2O, its formula weight is 325.12, and the CAS NO is 121268-17-5.

Alendronate sodium is a white, crystalline, nonhygroscopic powder. It is soluble in water, very slightly soluble in alcohol, and practically insoluble in chloroform. Alendronate sodium tablets for oral administration contain 91.37 mg of alendronate monosodium salt trihydrate, which is the molar equivalent of 70 mg of free acid, and the following inactive ingredients: microcrystalline cellulose, anhydrous lactose, croscarmellose sodium, and magnesium stearate.

Alendronate sodium is mainly used to cure following disease：

Prophylaxis and treatment of female osteoporosis
Treatment of male osteoporosis
Prevention and treatment of corticosteroid-associated osteoporosis together with supplements of calcium and vitamin D
Paget’s disease
Experimental treatment for Osteogenesis imperfecta

Alendronate sodium inhibits osteoclast-mediated bone-resorption. Like all bisphosphonates, it is chemically related to inorganic pyrophosphate, the endogenous regulator of bone turnover. But while pyrophosphate inhibits both osteoclastic bone resorption and the mineralization of the bone newly formed by osteoblasts, it specifically inhibits bone resorption without any effect on mineralization at pharmacologically achievable doses. Its inhibition of bone-resorption is dose-dependent and approximately 1,000 times stronger than the equimolar effect of the first bisphosphonate drug, etidronate.

Under therapy, normal bone tissue develops, and Alendronate sodium is deposited in the bone-matrix in pharmacologically inactive form. For optimal action, enough calcium and vitamin D are needed in the body in order to promote normal bone development. Hypocalcemia should, therefore, be corrected before starting therapy.

Etidronate has the same disadvantage as pyrophosphate in inhibiting mineralization, but all of the potent N-containing bisphosphonates including Alendronate sodium and also risedronate, ibandronate, and zoledronate, do not.

Before taking this medicine, tell your doctor or pharmacist if you are allergic to it; or to other bisphosphonates; or if you have any other allergies. Alendronate sodium may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.

Before using Alendronate sodium, tell your doctor or pharmacist your medical history, especially of: disorders of the esophagus (such as esophageal stricture or achalasia), trouble swallowing, trouble standing or sitting upright for at least 30 minutes, low calcium levels, stomach/intestinal disorders (such as ulcers).

Infrequently, people taking bisphosphonates have had serious jawbone problems (osteonecrosis). Poor dental hygiene, poorly fitting dentures, or having certain dental work.

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What is 3-Methyl-1-phenyl-2-pyrazolin-5-one?

3-Methyl-1-phenyl-2-pyrazolin-5-one (Radicut) is a neuroprotective agent used for the purpose of aiding neurological recovery following acute brain ischemia and subsequent cerebral infarction. It acts as a potent antioxidant and strongly scavenges free radicals, protecting against oxidative stress and neuronal apoptosis. It has been marketed solely in Japan by Mitsubishi Pharma since 2001. and marketed in India by Edinburgh Pharmaceuticals by the brand name Arone.

3-Methyl-1-phenyl-2-pyrazolin-5-one(A\CAS NO.:89-25-8) has been shown to attenuate methamphetamine- and 6-OHDA-induced dopaminergic neurotoxicity in the striatum and substantia nigra, and does not affect methamphetamine-induced dopamine release or hyperthermia.It has also been demonstrated to protect against MPTP-mediated dopaminergic neurotoxicity to the substantia nigra, though notably not to the striatum.

Reactive oxygen species play an important role in the pathogenesis of acute lung injury and pulmonary fibrosis. The present authors hypothesise that 3-Methyl-1-phenyl-2-pyrazolin-5-one, a free-radical scavenger, is able to attenuate bleomycin (BLM)-induced lung injury in mice by decreasing oxidative stress.

Lung injury was induced in female ICR mice by intratracheal instillation of 5mg·kg-1 of BLM. 3-Methyl-1-phenyl-2-pyrazolin-5-one (300 mg·kg-1) was administered by intraperitoneal administration 1 h before BLM challenge.

3-Methyl-1-phenyl-2-pyrazolin-5-one significantly improved the survival rate of mice treated with BLM from 25 to 90%, reduced the number of total cells and neutrophils in bronchoalveolar lavage fluid (BALF) on day 7, and attenuated the concentrations of lipid hydroperoxide in BALF and serum on day 2. The fibrotic change in the lung on day 28 was ameliorated by 3-Methyl-1-phenyl-2-pyrazolin-5-one, as evaluated by histological examination and measurement of hydroxyproline contents. In addition, 3-Methyl-1-phenyl-2-pyrazolin-5-one significantly increased the prostaglandin E2 concentration in BALF on day 2.

In summary, 3-Methyl-1-phenyl-2-pyrazolin-5-one was shown to inhibit lung injury and fibrosis via the repression of lipid hydroperoxide production and the elevation of prostaglandin E2 production in the present experimental murine system.

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Information you should know about Temozolomide

Temozolomide is an “alkylating agent” that links specific sections of DNA, thus preventing cell division and in turn, killing the cell. It is only FDA approved to treat brain cancer but it is also used “off label” in patients with melanoma that has metastasized (spread) to the brain or nervous system.

Although recent research has shown that temozolomide(CAS NO.: 85622-93-1) has a slightly higher response rate than the related chemotherapy drug dacarbazine, it didn’t improve the statistic that really counts: overall survival. However, since temozolomide comes in convenient pill form, some doctors prescribe it for patients who have difficulty with IV infusions or are unable to travel to a healthcare facility for the equally effective dacarbazine injection.

Evidence that Temozolomide is Effective

Temozolomide is only FDA approved to treat brain cancer but it is also used “off label” in patients with melanoma that has metastasized to the brain or nervous system.

In late 2008, Poulam Patel, Ph.D., and colleagues from the University of Nottingham in England presented results from a disappointing phase III trial that compared high doses of temozolomide to dacarbazine in patients with stage IV melanoma. Although temozolomide was shown to have a higher response rate than dacarbazine, it didn’t improve the statistic that really counts: overall survival. However, since temozolimide comes in convenient pill form, some doctors prescribe it for patients who have difficulty with IV infusions or are unable to travel to a healthcare facility for the equally effective dacarbazine injection.

Currently, 18 clinical trials are investigating temozolimide use in patients with metastatic melanoma. These include studies combining temozolimide with other drugs such as thalidomide and interferon-alfa2b. If you or a loved one has metastatic melanoma, be sure to ask your doctor if you are eligible for these trials.

Potential Side Effects

The following serious side effects have occurred in a small percentage of people taking temozolomide. If you experience any of these, seek emergency medical attention immediately:

Skin rash, itching or hives, pain at the injection site, swelling of the face, lips, or tongue (signs of an allergic reaction)
Fever or chills, cough, sore throat, pain or difficulty passing urine (signs of infection due to a decrease in the number of white blood cells)
Bruising, pinpoint red spots on the skin, black, tarry stools, blood in the urine (signs of a decreased number of platelets)
Severe weakness, fainting spells, lightheadedness (signs of a decreased number red blood cells)

The following less serious side effects of temozolomide have also been reported but don’t require immediate attention:

Nausea and vomiting, headache, fatigue, constipation, convulsions, numbness, insomnia, changes in vision, memory problems, problems with balance but walking, loss of appetite

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What diseases does Matrine cure

Matrine is an alkaloid found in plants from the Sophora genus. It has a variety of pharmacological effects, including anti-cancer effects, and action as a kappa opioid receptor and µ-receptor agonist.It is also have good function on Cardiac disease and Skin disease

Cancer

Matrineta(CAS NO: 519-02-8) has long been regarded an anticancer herb in China. According to cancer specialist Chang Minyi, “Matrineta works through stimulating the anticancer immune mechanism of the patient and reinforcing his resistance against the growth of the tumor.”

In 1998, Xu Xiangru and Jiang Jikai, working at the Congqing University of Medical Sciences, published a review of anticancer activity of Matrine. They relayed pharmacology studies indicating the alkaloids could inhibit growth of tumor cells directly, and could also affect immune functions.

In clinical work, they described the use of Matrine for treating the side effect of leukopenia caused by cancer chemotherapy or radiation therapy and for treating certain cancers, notably uterine cervical cancer and leukemia. The herb is also considered an important ingredient in treatment of esophageal and laryngeal cancer.

In a recent pharmacology study, it was reported that matrine could help leukemia cells differentiate into mature and normal white blood cells. Nonetheless, Matrine should not be relied upon as a sole treatment for cancer, but as an adjunct therapy, as there is no proof that the herb or these compounds are curative.

Cardiac disease

Matrine is commonly used in China for treatment of heart arrhythmias. A possible mechanism of action is to help block sodium and calcium channels, a mechanism relied on by several antiarrhythmic pharmaceuticals. In a review of Matrine effects on the heart, Li Yan and He Liren, at the Affiliated Yueyang Hospital of Shanghai University of TCM, reported that:

Matrine could counteract arrhythmia induced by many causes; it could regulate heart contractility; the total alkaloids could dilate the coronary artery, increase blood flow, and improve oxygen delivery to cardiac cells; and Matrine could counteract the coxsackie virus that causes myocarditis.

Li and He also relayed a clinical report from the Third Clinical Medical College of Beijing Medical University, about treatment of 167 patients with fast arrhythmia. The patients received each day 3-10 Matrine tablets (extract of 2 grams crude herb/tablet). The results indicated positive effects on various kinds of arrhythmia, such as premature systole, paroxysmal ventricular tachycardia, atrial fibrillation, and sinus tachycardia; the efficacy for premature systole appeared to be the best. This Beijing study and others were described also by Niu Kuizhi in his review of clinical applications of Matrine.

Skin disease

Matrine is frequently used in treatment of skin diseases, applied topically and consumed orally. One of the primary uses for topical therapy is treatment of vaginitis, particularly that due to candida infection . Recently, a topical liniment was developed combining Matrine’s matrine with the anti-inflammatory flavonoid baicalin from scute (huangqin) for treatment of eczema, neurodermatitis, and psoriasis.

This treatment was reported to be highly effective, especially for eczema, though the number of cases was small, so that further research must be done. The use of Matrine for psoriasis is a promising new area. Zhang Junling and his colleagues at the Department of Dermatology, Tianjin Changzheng Hospital, studied the mechanism by which Matrine reduce psoriasis patches. They found that the alkaloids could inhibit keratinocytes, the cells that reproduce continuously to produce the characteristic scales.

Side effects of Tacrolimus in 4 aspects

Tacrolimus is an immunosuppressive drug that is mainly used after allogeneic organ transplant to reduce the activity of the patient’s immune system and so lower the risk of organ rejection. It is also used in a topical preparation in the treatment of atopic dermatitis (eczema), severe refractory uveitis after bone marrow transplants, exacerbations of minimal change disease, and the skin condition vitiligo.

Tacrolimus(CAS NO.: 104987-11-3) is a 23-membered macrolide lactone discovered in 1984 from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis. It reduces interleukin-2 (IL-2) production by T-cells.

Preventing organ rejection in certain patients following liver, kidney, or heart transplant. It may be used along with other medicines. It may also be used for other conditions as determined by your doctor.Tacrolimus is an immunosuppressant. It blocks the action of certain blood cells (eg, T lymphocytes) that can cause the body to reject the transplanted organ. As a widely used medicine, Tacrolimus also has many side effects, in this article we will tall the side effect from 4 aspects:

From oral and intravenous administration

Side effects can be severe and include infection, cardiac damage, hypertension, blurred vision, liver and kidney problems (tacrolimus nephrotoxicity), hyperkalemia, hypomagnesemia, hyperglycemia, diabetes mellitus, itching, lung damage (sirolimus also causes lung damage),and various neuropsychiatric problems such as loss of appetite, insomnia, Posterior reversible encephalopathy syndrome, confusion, weakness, depression, cramps, neuropathy, seizures, tremors, and catatonia.

In addition it may potentially increase the severity of existing fungal or infectious conditions such as herpes zoster or polyoma viral infections.

Carcinogenesis and mutagenesis

In people receiving immunosuppressants to reduce transplant graft rejection, an increase risk of malignancy is a recognised complication. The most common cancers are non-Hodgkin’s lymphoma and skin cancers. The risk appears to be related to the intensity and duration of treatment.

From topical use

The most common adverse events associated with the use of topical tacrolimus ointments, especially if used over a wide area, include a burning or itching sensation on the initial applications, with increased sensitivity to sunlight and heat on the affected areas. Less common are flu-like symptoms, headache and cough and burning eyes.

The use of topical tacrolimus ointments should be avoided on known or suspected malignant lesions. The use of tacrolimus on patients with Netherton’s syndrome or similar skin diseases is not recommended. Patients should minimize or avoid natural or artificial sunlight exposure. Skin infections should be cleared prior to application, and there may be an increased risk of certain skin infections. Tacrolimus should not be used with occlusive dressings.

Cancer risks

Tacrolimus and a related drug for eczema (pimecrolimus) were suspected of carrying a cancer risk, though the matter is still a subject of controversy. The FDA issued a health warning in March 2005 for the drug, based on animal models and a small number of patients. Until further human studies yield more conclusive results, the FDA recommends that users be advised of the potential risks. However, current practice by UK dermatologists is not to consider this a significant real concern and they are increasingly recommending the use of these new drugs.

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