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Wednesday 31 May 2017

Chicken roti favourite is so big, it's 'two meals': The Dish

https://www.thestar.com/life/food_wine/2017/05/31/chicken-roti-from-alis-roti-shop-the-dish.html via @torontostar

Mississauga man helps swan keep nest afloat during flooding

 https://www.thestar.com/news/gta/2017/05/30/mississauga-man-helps-swan-keep-nest-afloat-during-flooding.html via @torontostar

Tuesday 30 May 2017

Re: Casperome®, a Frankincense Extract, Controls Minor Symptoms of Ulcerative Colitis in Remission

  • Boswellia (Boswellia serrata, Burseraceae)
  • Casperome®
  • Ulcerative Colitis
Date: 05-31-2017HC# 111635-569

Pellegrini L, Milano E, Franceschi F, et al. Managing ulcerative colitis in remission phase: usefulness of Casperome®, an innovative lecithin-based delivery system of Boswellia serrata extract. Eur Rev Med Pharmacol Sci. 2016;20(12):2695-2700.

Ulcerative colitis (UC), an inflammatory bowel disease, is characterized by various symptoms depending on the severity of inflammation and its location. Therapies range from topical therapy with 5-aminosalicylic acid (5-ASA) to treat active proctitis to topical and oral aminosalicylates for mild-to-moderate left-sided colitis and hospitalization and systemic therapy for severe left-sided colitis. The goal of treatment is to induce and maintain a remission phase and prevent disease- and treatment-related complications. For remission maintenance, the first-line therapy is 5-ASA administered orally or rectally. For mild cases of the disease, the benefits of long-term maintenance treatment are less certain. Herbal remedies could help manage mild UC during remission. Oleo-gum-resins from frankincense (Boswellia serrata, Burseraceae) have been used traditionally in India and Africa to treat various inflammatory diseases. The goal of this open-label, observational, registry study was to evaluate the efficacy of Casperome® (Indena SpA; Milan, Italy), a standardized frankincense extract, in patients with minimally symptomatic UC in remission phase.
Casperome is a lecithin-based delivery form of a highly purified standardized extract from the gum resin of frankincense and soy (Glycine max, Fabaceae) lecithin in a 1:1 ratio formulated with Phytosome® (Indena SpA; Milan, Italy) technology, which enhances absorption. It is standardized to contain ≥ 25% of triterpenoid acids.
The study, conducted in Italy, included 43 patients with clinically evaluated and confirmed UC who had been in remission for at least 1 year. Their symptoms were minimal, and they were not using any medications. The patients chose to receive the oral daily Casperome supplementation (n=22) or no supplementation (control group, n=21). The patients in the treatment group consumed one 250-mg Casperome tablet daily for 4 weeks.
At baseline and after 4 weeks, the following parameters were assessed: intestinal pain (ranging from no pain at 1 to continuous, severe pain at 5); bloody diarrhea, as number of episodes weekly; evacuation with blood and mucus, as episodes weekly; bowel movements, as episodes daily; intestinal cramps; suspected rectal involvement; watery stools; malaise; anemia; body weight; white blood cell count; need for specific drugs; and need of medical attention or hospitalization. A fecal immunochemical test was used to detect occult blood in stool samples, which were collected on alternate days. Bowel inflammation was assessed by determining the fecal concentration of calprotectin, an antimicrobial protein released in the intestinal lumen when inflammatory processes are present.
At baseline, all patients were similar in demographics and clinical characteristics. No safety or tolerability issues were observed during the study. Patients who left the study, 5 in the control group and 3 in the treatment group, did not do so for medical problems.
All tested parameters improved significantly after treatment with Casperome. Mild, diffuse intestinal pain and cramps decreased in intensity and frequency in the treatment group compared with the control group and compared with baseline (P<0.05). During the 4 weeks, the episodes of diarrhea, evacuations with blood/mucus, and number of bowel movements decreased in the treatment group compared with baseline and compared with the control group (P<0.05). The number of patients with suspected rectal involvement remained the same in the control group (13 patients) and decreased from 12 to 4 patients in the treatment group during the 4-week study (P<0.05). Anemia improved significantly in the treatment group from baseline to week 4 and compared with the control group (P<0.05).
In the treatment group, occult blood in the stool decreased during the 4 weeks. The number of patients with calprotectin levels in the stool > 100 μg/g totaled 19 (86.4%) in the treatment group and 18 (85.7%) in the control group at baseline. After 4 weeks, that number decreased significantly to 11 (50%) patients in the treatment group compared with 16 (76.2%) patients in the control group (P<0.05). Significant between-group differences were observed for the need for specific drugs (4 patients in the treatment group and 16 patients in the control group) and for the need for medical attention (9 in the control group and 4 in the treatment group) (P<0.05 for both measures).
Long-term treatment with 5-ASA drugs could have potential adverse effects and is costly. The authors conclude, "Despite all the limitations implicit in any observational analysis, our study demonstrated the Casperome®supplementation efficacy in controlling minor symptoms of UC in remission, and in reducing the use of drugs and medical consultation." Larger studies are needed to further evaluate these findings.
Three of the authors (E. Milano, F. Franceschi, and S. Togni) are employees of Indena SpA.
Shari Henson 

Re: Curcumin Improves Endothelial Function in Healthy, Young Subjects


  • Turmeric (Curcuma longa, Zingiberaceae)
  • Curcumin
  • Endothelial Function
  • Cardiovascular Disease Risk
Date: 05-31-2017HC# 101656-569

Oliver JM, Stoner L, Rowlands DS, et al. Novel form of curcumin improves endothelial function in young, healthy individuals: A double-blind placebo controlled study. J Nutr Metab. 2016;2016:1089653. doi: 10.1155/2016/1089653.

Damage to the vascular endothelium resulting in endothelial dysfunction has been implicated as an important mechanism in the development of cardiovascular disease (CVD). Curcumin extracts from turmeric (Curcuma longa, Zingiberaceae) rhizome have cardioprotective, antioxidant, and anti-inflammatory properties. Ex vivo, curcumin has been shown to reverse endothelial dysfunction, and one small (n = 32), randomized, controlled trial found curcumin supplementation for 8 weeks was comparable to exercise in improving endothelial function in postmenopausal women. According to the authors, there are no studies evaluating the effect of curcumin supplementation on endothelial function in healthy people. The purpose of this 8-week, randomized, placebo-controlled, double-blind study was to evaluate the effect of high and low doses of a proprietary curcumin supplement on endothelial function in healthy, young adults.
Healthy, nonsmoking men and women (n = 59, aged 19-29 years) participated in this study conducted in Fort Worth, Texas [study dates not reported]. Included subjects had no musculoskeletal, medical, or metabolic contraindications to exercise and did at least 150 min/week of moderate aerobic activity or 75 min/week of vigorous aerobic activity for the 3 months prior to enrollment. Excluded subjects were pregnant or lactating, participated in another clinical trial or consumed the investigational product within the previous 30 days, were regularly treated with anti-inflammatory/analgesic/antioxidant drugs in the previous month, or used any ergogenic aid during the 9 weeks prior to the study.
In this 3-arm trial, subjects received either placebo (corn [Zea mays, Poaceae] starch), 50 mg/day of curcumin (71.5% curcumin, 19.4% demethoxycurcumin, and 9.1% bisdemethoxycurcumin), or 200 mg/day of curcumin for 8 weeksThe curcumin treatments (CurcuWIN®; OmniActive Health Technologies Ltd.; Mumbai, India) were formulated with a hydrophilic carrier to improve absorption.
Subjects were told to abstain from eating foods that contain curcumin. At baseline and study end, fasting blood was drawn to assess safety, maximal aerobic capacity (treadmill test) was performed to control for the effect of exercise, and flow-mediated dilation (FMD) was assessed with sonography. FMD is a measure of endothelial function. A 1% increase in FMD was considered clinically relevant a priori.
The results of the blood analyses (complete blood count and metabolic panel) were within the normal range, and no adverse events were reported. The maximal aerobic capacity test verified that subjects' normal exercise routine did not affect endothelial function. The 200 mg/day dose significantly increased FMD (3%) compared to placebo (P < 0.032) and the increase was considered clinically meaningful (˃1%). Inference statistics also indicated that for the 200 mg/day dose, clinical benefit was likely with a benefit-to-harm ratio of 546:1.
The authors conclude that 200 mg/day of CurcuWIN for 8 weeks clinically and significantly increased FMD in healthy, young adults. As FMD is inversely associated with future cardiovascular events in healthy subjects, the authors suggest that curcumin may be "a simple lifestyle strategy for decreasing the risk of cardiovascular diseases in individuals who are apparently healthy." Further studies are needed to confirm whether the antioxidant and anti-inflammatory actions of curcumin are the mechanisms by which curcumin improves FMD. Limitations of this study include the small sample size, short study duration, and minimal reporting. Markers of inflammation and oxidative stress were not measured, and other CVD risk factors were not assessed or controlled for as variables in the statistical analyses. These results must be confirmed in a larger, longer-duration study using more rigorous methodology. The study was financially supported by OmniActive Health Technologies, the manufacturer of CurcuWIN.
—Heather S. Oliff, PhD 

Food as Medicine: Mustard (Brassica juncea and B. nigra, Brassicaceae)

HerbalEGram: Volume 14, Issue 3, March 2017


Editor’s Note: Each month, HerbalEGram highlights a conventional food and briefly explores its history, traditional uses, nutritional profile, and modern medicinal research. We also feature a nutritious recipe for an easy-to-prepare dish with each article to encourage readers to experience the extensive benefits of these whole foods. With this series, we hope our readers will gain a new appreciation for the foods they see at the supermarket and frequently include in their diets.
The basic materials for this series were compiled by dietetic interns from Texas State University in San Marcos and the University of Texas at Austin through the American Botanical Council’s (ABC’s) Dietetic Internship Program, led by ABC Education Coordinator Jenny Perez. We would like to acknowledge Perez, ABC Special Projects Director Gayle Engels, and ABC Chief Science Officer Stefan Gafner, PhD, for their contributions to this project.
By Hannah Baumana and Zachary Brownb
a HerbalGram Associate Editor
b ABC Dietetics Intern (TSU, 2015)
Overview
Mustard plants are herbaceous perennials (though often grown as annuals or biennials) and belong to the Brassicaceae, or cabbage, family.1 The three types of mustard most commonly consumed today are brown mustard (Brassica juncea), black mustard (B. nigra), and white mustard (Sinapis alba). This paper is concerned only with the brown and black species.
Native to temperate regions in Europe, mustard was one of the continent’s first domesticated crops, and thereafter became a cultivated food crop in Asia, North Africa, and North America.2 All species yield edible leaves, while their seeds are used whole, powdered, or pressed to produce oil.1 Annually, the United States produces 160,000 tons of mustard seed.3 Mustard plants have alternate leaves with ruffled margins and produce the small, yellow four-petaled flowers typical of members of the Brassicaceae family (formerly referred to as the Cruciferae family due to the cross-like pattern of the four petals). Upon pollination, each seedpod elongates into an oblong fruit capsule that contains up to 20 spherical seeds, which can be dark brown or yellow depending on the species.4
Black mustard is sparsely branched and erect. It grows up to three meters in height and produces very small, pungent seeds (1.5 grams per 1,000 seeds) that are shed by the plant as the seedpod matures.1 Black mustard is grown for its edible greens in Argentina, Chile, and the United States, but it is rarely cultivated as a seed crop due to difficulties with the harvesting process and has largely been replaced by brown mustard because of this. Brown mustard, also known as Indian or Oriental mustard, originated in the Himalayan region of central Asia. Brown mustard grows 1-2 meters tall, has larger seeds (three grams per 1,000 seeds), and produces seedpods that are easier to mechanically collect and process. Brown mustard is commercially grown in North America, specifically in parts of the United States and Canada.3
Phytochemicals and Constituents
Phytochemical differences in black mustard and brown mustard are minor, since B. juncea evolved from its ancestor B. nigra. The primary components of interest in mustard are the glucosinolates such as sinigrin, which are believed to be responsible for many of mustard’s health benefits.5 Mustard seed oil contains 90% allyl isothiocyanate (AITC). The seed contains 27% non-volatile oils (fixed oils), 30% proteins, and small amounts of lecithin, inositol, albumin, gums, mucilage, and pigments. Sinapine, an alkaloid, is also present in trace amounts. The fixed oils are composed of oleic, stearic, erucic, or brassic acids. Mustard seeds also contain terpenes, which have anti-inflammatory properties and are the primary constituents of mustard essential oil.
Other constituents in significant amounts include flavonoids and other phenolic compounds. The concentrations of these compounds can vary widely based on the growing conditions of the mustard plant. Pathogenic attacks on the plant also result in an altered phytochemical profile. Thus, it is possible that the health effects of mustard can vary due to the different farming practices used to grow the mustard. It would be beneficial to standardize farming practices to maximize yields of specific plant chemicals.6
Mustard greens are nutrient dense and contain high amounts of vitamins, such as vitamin A, vitamin K, and vitamin C, and minerals, such as calcium. Mustard seeds contain fewer vitamins but are a good source of iron, calcium, magnesium, and other minerals. Mustard seeds are also a good source of omega fatty acids, as they contain an almost 1:1 ratio of omega-3 and omega-6 fatty acids. Both the seeds and greens can offer health-protective effects through their impressive nutrient profiles, although prepared mustard as a condiment should be used sparingly, since many commercial brands can contain high amounts of sodium.1
Historical and Commercial Uses
The recorded use of mustard as a medicinal plant dates back to the first century CE in Greece, where the physician Dioscorides recommended the topical application of a mustard seed poultice to reduce inflammation in his herbal medicine encyclopedia De Materia Medica.7 In Unani literature (the Greco-Arabic system of traditional medicine), mustard seed is recommended for a variety of conditions, including neuralgia, epilepsy, sciatica, leprosy, gout, pleurisy, and pneumonia.5
In Ayurveda, the system of traditional medicine practiced for thousands of years in India, the therapeutic uses of mustard are well documented. The Ayurvedic practice considers mustard seed oil derived from the brown mustard plant to be pungent and warming, and documents external uses such as a massage oil and a hair tonic; for skin diseases like vitiligo; skin infections like acne; and hemorrhoids.8 Mustard seeds were processed into a paste and used as a poultice to treat internal conditions such as tumors of the thyroid gland and lymphadenitis (swelling of lymph nodes). Mustard seeds were also decocted in water and used as a poultice for cracked skin, leprosy, rheumatoid arthritis, acne, and as a rinse for mouth sores.
Internally, mustard oil traditionally was used to lower blood lipid levels, reduce build-up of fat or adipose tissue, treat intestinal worms, and assist detoxification of the body. Mustard seeds were also included in traditional herbal formulas used to induce vomiting and cleanse the cranial cavity via nasal irrigation, and as a decoction in an enema therapy.8 Though mustard leaves were more commonly consumed as a vegetable, they were also used as an ingredient for steam fomentation and to cleanse the cranial cavity.
Other ethnobotanical uses of the mustard plant exist in cultures around the world.1 In Africa, the roots are used as a galactagogue to stimulate milk production. Dried leaves and flowers are burned in Tanzania in spiritual rituals. The essential oil has been used to relieve constipation and as a counterirritant. In Java, the leaves are used internally to treat syphilis and stimulate blood flow to the pelvic area and topically to treat headaches. In Korea, the seeds are used for abscesses, colds, lower back pain, rheumatism, and stomach disorders. The oil of mustard has been used to treat skin eruptions and ulcers throughout Asia.
In North America, black mustard has a history of use among indigenous tribes.9 It was used by the Cherokee to stimulate the appetite, treat fever and “nervous fever,” heal the kidneys, and treat various other diseases such as malaria. It was also used to treat palsy and asthma, and as a tonic for overall wellness. The Meskwaki used mustard due to its pungent nature to treat head colds. The Mohegan tribe applied mustard leaf poultices as an analgesic for body pains, headaches, and toothaches. The Shinnecock used it similarly to the Mohegan, but also mixed it with flour and water to induce vomiting. Brown mustard seed powder also has a widespread use as an emetic to treat acute and narcotic poisoning.10
Modern Research
In recent studies, mustard has shown antitumor effects and other beneficial properties against chronic conditions, including diabetes, cardiovascular disease, weight gain, and neuropathic disease. It might also act as a protective agent against acute conditions such as fungal infection and influenza.
Cytotoxic and Anti-Tumor Effects
The anticancer effect of mustard may be due to the anti-proliferative activity of constituents such as sinigrin, the precursor to AITC. Many cytotoxicity studies have been performed in vitro to investigate how mustard and its constituents act against cancer cell proliferation. A hydrolyzed mustard seed powder that contained AITC caused cell cycle arrest and apoptosis (programmed cell death) in bladder cancer cell lines.11 This was further observed in rats, where an oral dose of the hydrolyzed mustard seed powder inhibited bladder cancer growth and blocked muscle invasion of cancerous cells. AITC specifically is thought to be selectively delivered to the bladder through urinary excretion. The mustard powder produced more significant results than pure AITC, suggesting that ingestion of the whole seed is more beneficial than ingestion of any isolated constituents. In an animal model, injections of mustard essential oil rich in AITC inhibited cell proliferation and blood vessel creation (angiogenesis, which is required for tumor growth).12The oil also induced apoptosis, a pathway for cancer chemoprevention.
Another study examined the effects of sinigrin on liver tumors in rats. This three-month study found that oral sinigrin administration significantly inhibited proliferation of tumor cells in the liver and reduced the number of tumors in the rat liver. The response was dose dependent, with the highest tumor suppression at 25 mg/kg of body weight. However, the lowest dose, 10 mg/kg, still caused a significant reduction of tumors on the liver surface compared to the positive control, reducing tumor size by half.13
An in vitro study examined the effects of several mustard extracts and found a dose-dependent protective response in human hepatocytes, colorectal cells, cervical cells, breast cancer cells, and larynx cells.5 The juice of the mustard leaf was also found to protect against induced DNA damage in human cells, again in a dose-dependent manner. These cancer chemopreventive effects were thought to be mediated not through inherent antioxidant properties of mustard extract, as is often seen with many plant materials, but by increasing expression of detoxification enzymes.
Isothiocyanates may also decrease multidrug resistance in human cancer cell lines and inhibit the efflux (simply put, the removal of compounds from cells) of cancer-treating drugs, which enhances the effect of chemotherapy treatment. In an in vitro study, isolated compounds, including isothiocyanates and sulforaphane, increased the accumulation of chemotherapeutic drugs in multidrug resistant cancer cells through the inhibition of efflux of these drugs.14 Researchers also found that the isothiocyanates inhibited tumor formation in breast, colon, lung, and skin tissue.
Diabetes, Cardiovascular Disease, and Neuropathic Effects
Mustard leaves and seeds both can induce hypoglycemic effects in animals with type 2 diabetes. One rodent study found that administration of an extract made from mustard leaves significantly reduced lipid peroxidation, reduced free radicals, and ameliorated the damage caused by oxidative stress.15 Researchers speculated that mustard enhances glycolysis and glycogenesis, and decreases glycogenosis. These data were further confirmed by a follow-up study that also showed reduced levels of superoxide and nitrite/nitrates in a dose-dependent manner after oral administration of a mustard extract.16 Mustard may also delay or prevent the onset of diabetes in addition to mitigating its effects. A study examined the effects of feeding high-fructose diets to rodents for 30 days and found that the inclusion of mustard powder over the study period significantly decreased fasting serum glucose, insulin, and cholesterol levels, although not enough to normalize them.17 Researchers concluded that mustard powder may be beneficial for pre-diabetic patients and those who are genetically prone to the disease.
Cardiovascular disease (CVD) is often studied in tandem with diabetes, as individuals with diabetes tend to suffer from CVD as well. One study examined the effects of two doses of mustard seed powder on serum cholesterol and triglycerides in diabetic rats.18 The lower dose did not significantly affect these markers; however, a higher dose (8 g/kg of body weight) significantly and consistently lowered both. The authors suggested that mustard might mimic or enhance the effectiveness of insulin, lowering the necessary amount and reducing insulin’s anabolic effect.
There are often neurological complications associated with diabetes. In a rat model, researchers examined the effects of an ethanol mustard extract and found dose-dependent improvements in brain chemistry and cognitive function, and speculated that non-diabeties-induced neurological problems could be improved with mustard consumption or supplementation.19 The effect of mustard on the depletion of neurotransmitters norepinephrine, serotonin, and dopamine was further researched.20 Mustard was found to compensate for depleted levels of neurotransmitters in the brain, resulting in improvement of behavioral outcomes such as feelings of helplessness and despair, as well as impaired locomotion. Mustard’s rich polyphenol content may be the source of its therapeutic effects on cognitive issues.
Antimicrobial Properties
Mustard has antimicrobial and antiviral properties and shows protective effects against microbe- and virus-induced damage. One rodent study on viral hepatitis found that mustard extract protected against liver and kidney damage. The mechanism of this protective action is thought to be related to the anti-inflammatory activity of the compounds in mustard such as terpenes.21 This is of specific interest because it shows that the protective properties of mustard go beyond antibiotic properties and may protect against viruses as well.
Mustard has also been shown to have antifungal properties. Mustard essential oil was able to inhibit or delay the growth of several types of fungi and prevent further growth even if mustard essential oil was in contact with the fungi through vapors.22 Furthermore, mustard was found to recognize the structural differences of microbes and targeted sphingolipids, specific regulators of pathogenicity unique to fungal pathogens.23
Consumer Considerations
Mustard as a food generally is considered safe. There are no known nutrient-drug interactions with mustard, although high levels of vitamin K in the leaves could interact with certain blood-thinning medications such as warfarin due to vitamin K’s blood-coagulating properties. The vitamin K content could also be a concern to individuals with existing untreated thyroid issues or an iodine deficiency. Due to the high oxalate content of the leaves, those with a history of oxalate-containing kidney stones may wish to limit their intake of mustard leaves.24
Mustard essential oil can be highly irritable to the skin and mucous membranes. It is not recommended to use mustard oil either internally or externally. However, mustard oil must be specifically extracted and these side effects are not a concern when consuming the condiment, seeds, or leaves.25 While there is little concern about adulteration of culinary mustard, there is a history of adulterating mustard seed oil with argemone (Argemone mexicana, Papaveraceae) oil. In 1998, 2,300 people were affected and 41 people died from adulterated mustard oil in India, resulting in a complete ban of mustard seed oil.26 The ban was subsequently lifted after the adulteration was discovered and corrected. However, mustard seed oil for edible consumption is not recognized as safe in the United States, Canada, and European Union due to its high erucic acid content.27
Nutrient Profile28
Macronutrient Profile: (Per 1 cup [approx. 56 grams] chopped mustard greens, raw)
15 calories
1.6 g protein
2.6 g carbohydrate
0.2 g fat

Secondary Metabolites: (Per 1 cup [approx. 56 grams] chopped mustard greens, raw)
Excellent source of:
Vitamin K: 144.2 mcg (180.3% DV)
Vitamin C: 39.2 mg (65.3% DV)
Vitamin A: 1,693 IU (33.9% DV)
Very good source of:
Manganese: 0.3 mg (15% DV)
Good source of:
Dietary Fiber: 1.8 g (7.2% DV)
Calcium: 64 mg (6.4% DV)
Potassium: 215 mg (6.1% DV)
Vitamin E: 1.13 mg (5.6% DV)
Iron: 0.92 mg (5.1% DV)
Also provides:
Vitamin B6: 0.1 mg (5% DV)
Magnesium: 18 mg (4.5% DV)
Riboflavin: 0.06 mg (3.5% DV)
Thiamin: 0.05 mg (3.3% DV)
Phosphorus: 32 mg (3.2% DV)
Niacin: 0.45 mg (2.3% DV)
Folate: 7 mcg (1.8% DV)
DV = Daily Value as established by the US Food and Drug Administration, based on a 2,000-calorie diet.

Recipe: Saag Paneer
Adapted from Anita Jaisinghani29
Ingredients:
  • 1/4 cup ghee or neutral vegetable oil, divided
  • 1 medium yellow onion, chopped
  • Salt and pepper to taste
  • 3 garlic cloves, minced
  • 2 serrano chilies, stems and seeds removed, minced
  • 2-inch piece of ginger, peeled and minced/grated
  • 1 pound of mustard greens, stems removed and leaves chopped
  • 1 pound baby spinach leaves
  • 2 teaspoons garam masala spice blend
  • 3/4 cup heavy cream or plain, unsweetened yogurt
  • 1 pound paneer or halloumi cheese, diced into 1-inch pieces
Directions:
  1. In a large saucepan, heat 3 tablespoons of the ghee or oil. Add the onion and season with salt and pepper. Cook over moderately low heat, stirring occasionally, until soft and golden brown, about 20 minutes.
  2. Add the garlic, chilies, and ginger. Cook over moderate heat, stirring occasionally, until softened, about 5 minutes. Stir in the garam masala and cook until fragrant.
  3. In batches, add the mustard greens and spinach, letting each batch wilt before adding more. Season with salt and pepper.
  4. In a food processor, pulse half of the greens with half of the heavy cream or yogurt until finely chopped. Return to the saucepan and repeat with the remaining greens and cream/yogurt. Alternatively, use an immersion blender to process the greens and dairy in the saucepan. Keep the saag warm over very low heat, stirring occasionally.
  5. In a medium nonstick skillet, heat 1/2 tablespoon of the ghee or oil over moderate heat. Add half of the paneer and cook, turning once, until golden brown, about 5 minutes. Transfer to a paper towel-lined plate to drain. Repeat with the remaining ghee and paneer.
  6. Fold the paneer into the saag and cook over low heat until warmed through, 2 to 3 minutes. Season with salt and pepper. Serve with steamed basmati rice.

References
  1. Duke J. Handbook of Energy Crops. Unpublished; 1983. Available at: https://hort.purdue.edu/newcrop/duke_energy/Brassica_juncea.html. Accessed February 15, 2017.
  2. Oplinger E, Oelke EA, Putnam DH, et al. Mustard. Alternative Field Crops Manual. Madison, WI and St. Paul, MN: University of Wisconsin Department of Agronomy and University of Minnesota Center for Alternative Plant and Animal Products; 1991. Available at: https://hort.purdue.edu/newcrop/afcm/mustard.html. Accessed February 15, 2017.
  3. Van Wyk B-E. Food Plants of the World. Portland, Oregon: Timber Press; 2005.
  4. Brassica juncea. Missouri Botanical Garden website. Available at: www.missouribotanicalgarden.org/PlantFinder/PlantFinderDetails.aspx?kempercode=a669. Accessed February 15, 2017.
  5. Nauman S, Mohammad I. Role of khardal (Brassica nigra) in non-communicable diseases: an overview. Int J Drug Dev Res. 2015;7(1):137-144.
  6. Kumar V, Thakur AK, Barothia ND, Chatterjee SS. Therapeutic potentials of Brassica juncea: an overview. International Journal of Genuine Traditional Medicine. 2011;1(1):1-17. http://dx.doi.org/10.5667/tang.2011.0005.
  7. Dioscorides P. De Materia Medica [trans. Osbaldeston TA]. Johannesburg, South Africa: IBIDIS Press; 2000.
  8. Manohar R, Pushpan R, Rohini S. Mustard and its uses in Ayurveda. Indian Journal of Traditional Knowledge. 2009;8(3):400-404.
  9. Moerman D. Native American Medicinal Plants: An Ethnobotanical Dictionary. Portland, Oregon: Timber Press; 2009.
  10. Lewis WH, Elvin-Lewis MPF. Medical Botany: Plants Affecting Human Health. 2nd ed. Hoboken, NJ: John Wiley & Sons; 2003.
  11. Bhattacharya A, Li Y, Wade KL, Paonessa JD, Fahey JW, Zhang Y. Allyl isothiocyanate-rich mustard seed powder inhibits bladder cancer growth and muscle invasion. Carcinogenesis. Dec 2010;31(12):2105-2110. doi:10.1093/carcin/bgq202/.
  12. Kumar A, D’Souza SS, Tickoo S, Salimath BP, Singh HB. Antiangiogenic and proapoptotic activities of allyl isothiocyanate inhibit ascites tumor growth in vivo. Integr Cancer Ther. 2009;8(1):75-87. doi:10.1177/1534735408330716.
  13. Jie M, Cheung WM, Yu V, Zhou Y, Tong PH, Ho JWS. Anti-proliferative activities of sinigrin on carcinogen-induced hepatotoxicity in rats. PLoS One. 2014;9(10):e110145. doi:10.1371/journal.pone.0110145.
  14. Tseng E, Kamath A, Morris M. Effect of organic isothiocyanates on the P-glycoprotein- and MRP1-mediated transport of daunomycin and vinblastine. Pharm Res. 2002;19(10):1509-1515.
  15. Kim HY, Yokozawa T, Cho EJ, Cheigh HS, Choi JS, Chung HY. In vitro and in vivo antioxidant effects of mustard leaf (Brassica juncea). Phyto Res. 2003;17(5):465-471. doi:10.1002/ptr.1174.
  16. Yokozawa T, Kim HY, Cho EJ, Yamabe N, Choi JS. Protective effects of mustard leaf (Brassica juncea) against diabetic oxidative stress. J Nutr Sci Vitaminol (Tokyo). 2003;49:87-93.
  17. Yadav SP, Vats V, Ammini AC, Grover JK. Brassica juncea (rai) significantly prevented the development of insulin resistance in rats fed fructose-enriched diet. J Ethnopharmacol. 2004;93(1):113-116.
  18. John P., Aravindakshan CM. Hypolipidemic effect of Brassica juncea (mustard) in alloxan induced diabetic rats. JIVA. 2012;10(2):13-16.
  19. Thakur AK, Chatterjee SS, Kumar V. Beneficial effects of Brassica juncea on cognitive function in rats. Pharm Biol. 2013;51(10):1304-1310. doi:10.3109/13880209.2013.789917.
  20. Thakur A., Chatterjee S., Kumar V. Antidepressant-like effects of Brassica junea L. leaves in diabetic rodents. Ind J Exp Biol. 2014;52:613-622.
  21. Rajamurugan R, Suyavaran A, Selvaganabathy N, et al. Brassica nigra plays a remedy role in hepatic and renal damage. Pharm Biol. 2012;50(12):1488-1497. doi:10.3109/13880209.2012.685129.
  22. Mejía-Garibay B, Palou E, López-Malo A. Composition, diffusion, and antifungal activity of black mustard (Brassica nigra) essential oil when applied by direct addition or vapor contact. J Food Prot. 2015;78(4):843-848.
  23. Oguro Y, Yamazaki H, Takagi M, Takaku H. Antifungal activity of plant defensin AFP1 in Brassica juncea involves the recognition of the methyl residue in glucosylceramide of target pathogen Candida albicansCurrent Genet. 2014;60(2):89-97.
  24. Murray M, Pizzorno J, Pizzorno L. The Encyclopedia of Healing Foods. New York, New York: Atria Books; 2014.
  25. Tisserand T, Young R. Essential Oil Safety. 2nd ed. London, UK: Churchill Livingstone; 2014.
  26. Babu CK, Khanna SK, Das M. Adulteration of mustard cooking oil with argemone oil: do Indian food regulatory policies and antioxidant therapy both need revisitation? Antioxid Redox Signal. 2007;9(4):515-525.
  27. Agriculture and Consumer Protection. SECTION 2: Codex Standards for Fats and Oils from Vegetable Sources. Food and Agriculture Organization of the United Nations. 1999. Available at: www.fao.org/docrep/004/y2774e/y2774e04.htm. Accessed February 22, 2017.
  28. Basic report: 11270, mustard greens, raw. United States Department of Agriculture Agricultural Research Service Available at: https://ndb.nal.usda.gov/ndb/foods/show/3018. Accessed February 22, 2017.
  29. Jaisinghani A. Mustard Greens Saag Paneer. Food and Wine. January 2017. Available at: www.foodandwine.com/recipes/mustard-greens-saag-paneer. Accessed February 22, 2017.

Contributions to conservation outcomes by natural history museum-led citizen science: Examining evidence and next steps

https://www.researchgate.net/publication/309163937_Contributions_to_conservation_outcomes_by_natural_history_museum-led_citizen_science_Examining_evidence_and_next_steps

Posted: 30 May 2017 06:56 AM PDT
The Orchid Observers project has been cited in a journal article and book chapter, both co-authored by Dr John Tweddle, Head of the Angela Marmont Centre for UK Biodiversity, Natural History Museum London.
Orchid Observers is one of the projects analysed in Contributions to Conservation Outcomes by Natural History Museum-led Citizen Science: Examining Evidence and Next Steps. The article was published in Biological Conservation, Volume 208, April 2017 pages 87-97 and is available to read here.
Orchid Observers is cited as an innovation case study in the chapter Citizen Science: Authentic Science Research at the Natural History Museum, In: Museum Participation: New Directions ForAudience Collaboration, edited by Kayte McSweeney and Jen Kavanagh.  (Published April 2016).

Sunday 28 May 2017

Letrozole, berberine, or a combination for infertility in Chinese women with polycystic ovary syndrome: a multicentre, randomised, double-blind, placebo-controlled trial

Abstract

Background

Letrozole is superior to clomiphene in infertile women with polycystic ovary syndrome and leads to higher ovulation and live birth rates. Berberine, a major active component of Chinese herbal medicine Rhizoma coptidis and found in Cortex Phellodendri and Cortex Berberidis in the rest of the world, has similar but even more profound metabolic effects than metformin. Our hypothesis was that a combination of letrozole and berberine would result in a higher live birth rate than letrozole or berberine alone in infertile women with polycystic ovary syndrome.

Methods

In this multicentre, randomised, double-blind, placebo-controlled trial in 19 participating centres in mainland China, we compared the effect of three interventions for up to six menstrual cycles: letrozole plus berberine placebo (letrozole group), berberine plus letrozole placebo (berberine group), or the combination of letrozole and berberine (combination group). The randomisation (1:1:1) was done through a web-based computer program operated by an independent data center in the China Academy of Chinese Medical Sciences. Participants, investigators, doctors, laboratory technicians, and data analysers were masked to the assignments. Eligible women (age 20–40 years) had polycystic ovary syndrome, as defined by the Rotterdam criteria, had at least one open Fallopian tube and normal uterine cavity, and had at least 1 year of infertility. Berberine or berberine placebo were administrated orally at a daily dose of 1·5 g for 6 months. Patients received an initial dose of 2·5 mg of letrozole or placebo on days 3–7 of the first three treatment cycles. This dose was increased to 5 mg letrozole or placebo on days 3–7 of the last three treatment cycles if not pregnant. Couples were instructed to have regular intercourse two to three times a week until becoming pregnant. The primary outcome was live birth rate after intervention for up to six menstrual cycles. We used either a χ2 test or Fisher's exact test a two-sided significance level of 0·05 to test differences between groups. Data were analysed according to the intention-to-treat principle. This study was approved by an Ethics Committee (2009LL-001) at First Affiliated Hospital in Heilongjiang University of Chinese Medicine. This trial is registered at Chinese Clinical Trials Registration, identifier ChiCTR-TRC-09000376, and at ClinicalTrials.gov, number NCT01116167. All participants provided written informed consent.

Findings

We enrolled 644 participants. The live birth rates were comparable between the letrozole group (78 [36%] of 215 births) and the combination group (74 [34%] of 215 birth) after treatment (odds ratio [OR] 0·92, 95% CI 0·62–1·37; p=0·687), whereas live birth rates in the berberine group (44 [22%] of 214 births) were lower than in the letrozole group (OR 2·02, 95% CI 1·32–3·10; p=0·001) and the combination group (OR 1·86, 95% CI 1·21–2·86; p=0·004). Conception, pregnancy, and ovulation rates were similar in the letrozole (46%, 39%, and 59%, respectively) and combination groups (49%, 38%, and 61%, respectively), and these were higher than in the berberine group. There was one twin birth in the letrozole group and three twin births in the combination group, but none in the berberine group (29%, 22%, and 6%, respecitively). Berberine was associated with constipation and nausea whereas letrozole was associated with fatigue and hot flashes.

Interpretation

For ovulation and live births, the combination of letrozole and berberine did not improve outcomes compared with letrozole alone, but letrozole and the combination of letrozole and berberine improved fertility in women with polycystic ovary syndrome compared with berberine alone. Some limitations include the early study termination because of the expiration of the study drug berberine or placebo, not all participants had pelvic sonograms to assess for polycystic ovaries, and some participants had regular cycles. The major strength of this study is that it was a large multicentre, double-blind trial with close monitoring of adverse events and serious adverse events and tracking of live birth in line with our recent Harbin consensus.

Funding

National Public Welfare Projects for Chinese Medicine (200807021) of China, the National Key Discipline of Chinese Medicine in Gynecology during the year of 2009–14, the Heilongjiang Province Foundation for Outstanding Youths (JC200804), the Intervention for Polycystic Ovary Syndrome Based on Traditional Chinese Medicine Theory—‘TianGui Shi Xu’ (2011TD006), and the National Clinical Trial Base in Chinese Medicine during the year of 2009–14 in First Affiliated Hospital, Heilongjiang University of Chinese Medicine.
Declaration of interests
All authors report financial support to their institutions from the National Public Welfare Projects for Chinese Medicine of China and the National Key Discipline of Chinese Medicine in Gynecology during the year of 2009–14. X-KW reports other research grants for this trial from the Heilongjiang Province Foundation for Outstanding Youths and the Intervention for Polycystic Ovary Syndrome Based on Traditional Chinese Medicine Theory—‘TianGui Shi Xu’. ES-V reports a travel grant from Longjiang Scholarship from Heilongjiang Province. X-KW, EHYN, J-PL, and ES-V are members of the Steering Committee and received conference travel expenses and lecture fees from National Key Discipline of China. YX and YW are members of the Scientific Advisory Board, and have received payment from National Key Discipline and TCM Trial Base of China.
Acknowledgments
We thank the participants and the staff of participating centres for their contribution to the trial. This work was a post-doctoral dissertation of Xiao-Ke Wu MD

Supplementary Material

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pdf iconSupplementary appendixpdf.09 MB

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1897: Superhero Policeman Fogarty and the Crime-Stopping Goats of East Harlem


Posted: 21st March 2014 by The Hatching Cat in Goats of New York
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Central Park, 1880
On the border of Central Park, circa 1880. Collection of the Museum of the City of New York, Image ID: 805713
The following story is dedicated in memory of the eight people who died in a building collapse in East Harlem, when a leak in a natural gas pipeline laid in 1887 exploded on March 10, 2014.
If you’ve read Edith Wharton’s “The Age of Innocence,” you may recall her describing “the one-story saloons, the wooden greenhouses in ragged gardens, the rocks from which goats surveyed the scene” near Mrs. Manson Mingott’s white marble row house on Fifth Avenue.
Edith Wharton House
The white marble row house built by Edith Wharton’s great-aunt Mary Mason Jones, looking south from 58th Street in 1899. Photo: Office for Metropolitan History
Although the novel is fiction, much of the story is based on Edith’s own life and experiences in old New York. Mrs. Mingott’s house was based on the real home that Edith’s great-aunt Mary Mason Jones built in 1899. The wooden structures, rocks and goats were also very real in the 1800s.
Walking through the streets of New York City today, it’s hard to believe that only 100 years ago Upper Manhattan was sparsely developed, save for some rickety shantytowns where squatters of mostly Irish or Italian descent lived among the communal goats and chickens.
To be sure, there were a few luxury apartment buildings and tenements here and there – the Dakota at 72nd Street among the most notable – but they were few and far between.
The Dakota, 1889
This illustration of the Dakota at 72nd Street from Frank Leslie’s Illustrated Paper, September 7, 1889, depicts the typical squatters’ shantytown of the Upper West Side.
The Goats of Harlem
During the 1800s, the Upper West Side of Manhattan from about 59th Street to Harlem was known as Goat Town or Goatville. Before the extension of the Eighth Avenue elevated railroad prompted new housing construction above Central Park, there was an estimated 15,000 goats in Goat Town.
There were also many goats roaming free on the Upper East Side, especially before some well-to-do residents of Yorkville and East Harlem formed the Anti-Goat Protective Association to expel the goats in 1884.
Eighth Avenue El, late 1800s
The Eighth Avenue elevated railroad, probably just north of 116th Street. As farmers sold their land, the lots were raised to the new street level.
Although most of Harlem’s goats received bad press for creating a nuisance – like entering a parlor window and devouring wall hangings or trampling flower gardens — the goats in the following story helped the police solve a crime.
Harlem Map, First Avenue
The Harlem Market Company leased 14 acres between 102nd and 103rd Street, First Avenue, and the East River. Existing buildings were converted to booths and new sheds (blue) were constructed to shelter the horse teams.

The Thieves of the Harlem Market

The Harlem Market, one of the greatest open-air markets of its time, was started by a group of men who wanted to provide a wholesale market for small tradesmen and farmers from Westchester County and Long Island. The men, led by M. Michael, J. Wulfhop, E. Williams, and H.C. Koster, established the Harlem Market Company in 1891 with a capital stock of $50,000.
Harlem Market
The Harlem Market during the transition from horse-drawn wagons (bottom left) to motorized trucks. New York Public Library, Image ID: 416550
All along First Avenue, blacksmiths and wagon repairmen opened shops to provide new shoes for the horses and fix carriages that suffered damages making the long journey from the farms to the market. Hotels and saloons also sprang up to provide services for the farmers. Hundreds of wagons arrived each day, many of them via steam ferry from College Point, Queens, to 99th Street or the new (1894) Public Services ferry from Edgewater, NJ, to 125th Street.
On November 20, 1897, two men from East 70th Street decided to try their luck at the Harlem Market, which was packed that Friday morning with wholesale wagons and retail push-carts. They loaded their light wagon with some stolen produce, including a crate of onions, a box of oranges, and a basket of string beans. Unbeknownst to them, however, the basket of beans had a hole in it.
Bicycle Policeman Daniel J. Fogarty
Bicycle Policeman Daniel J. Fogarty of the East 104th Street police station.
When the owners discovered the loss shortly thereafter, they summoned Bicycle Policeman Fogarty. There was no good description of the thieves, so where was he to begin? Perhaps the procession of goats following a trail of beans on the ground held the answer.
Fogarty followed the goats, which led him to the first thief, Joseph Abrams, 26. While the owner was identifying his produce, Abraham Yansky, 22, began to protest the arrest. The victim identified Yansky as Abrams’ accomplice, and he was also arrested. Both men were brought to the Harlem Police Court and held for trial on what was then a pretty stiff bail for stealing some fruit — $200.
Harlem Court House
The Harlem Courthouse at 170 East 121st Street and Sylvan Place was designed by Arthur M. Thom and James W. Wilson and completed in 1893. The brick, brownstone, bluestone, granite and terra-cotta building was built for the Municipal and Magistrate’s Courts, and included the Fifth District Prison. Today the landmark building is occupied by the Harlem Community Justice Center.
The Superhero of East Harlem
Although this story was originally going to be a quick and silly one about some goats, as I dug deeper into the career of Bicycle Policeman Daniel Fogarty, the story got longer – but much more amazing.
During his early career, Policeman Daniel Fogarty was stationed at the East 104th Street police station, which had jurisdiction from East 96th Street to East 116th Street, and from Central Park (and from Sixth Avenue above 110th Street) to the East River, as well as Ward’s Island. It turns out that Policeman Fogarty was a real superhero of East Harlem, a sort of Batman on two wheels in the late 19th century.
The 28th Police Precinct Station House
The 28th Police Precinct Station House was located at 177 East 104th Street between Lexington and Third Avenues. The five-story station house, which had a two-story prison and lodging house in the rear of the lot, was designed by renowned NYPD architect Nathaniel D. Bush and completed in 1893. It opened on June 28, 1893, and closed in 1974 (then the 23rd Precinct).
The New York press loved writing about his courageous adventures, whether he was being dragged along the ground while trying to stop runaway horses, jumping into the ice-cold river to save drowning victims, or pulling children from harm’s way in the nick of time.
Sergeant Daniel J. Fogarty
In his 19 years of service, Policeman Fogarty won eight life-saving medals, including a gold medal from Congress for saving a man in the Harlem River. As a friend once told the press, Fogarty had “enough medals to make the German Emperor look like a bloomin’ civilian.”
Here’s just a brief summary of some of his more daring rescues:
January 1896:
Just three months after leaving the postal service to join the police department, Policeman Fogarty rescued a Roman Catholic priest who had fallen from a pier into the icy Harlem River. Shortly after this incident, he jumped into the East River to save Johnnie Crowe, a little boy who had fallen from his mother’s lap into the East River at the Peck Slip pier. The strong current carried them to the Brooklyn Bridge, where a tugboat picked them up.
West Farms trolley car
While riding on a West Farms trolley car (like seen here) in July 1896, Policeman Fogarty saw James Harvey fall into the Harlem River. He jumped from the moving trolley, dove off the old Harlem Bridge, and swam 150 feet to rescue Harvey. Fogarty lost two revolvers in the river. (Anyone want to go scuba diving in the Harlem River?)
January 1898:
While cycling down First Avenue around 11 p.m., Daniel heard cries for help coming from the river near 98th Street. He blew his whistle for help, charged into the icy water – striking his leg on a spike – and attempted to rescue William O’Toole, a fireman on the steamship Saratoga who had probably been drinking at Gregory Moser’s barroom. Hearing the struggle, Policemen Darrow and Maguire ambushed the No. 19 horse car and grabbed the reins from the driver’s hands. With some help from a few passengers, they were able to use the cut reins to pull the men from the river.
Asked by a reporter why he thought it was okay for a bicycle policeman to rescue a sailor from the river, Daniel said his book of rules wasn’t handy, so he just guessed it was the right thing to do.
May 1899:
Seeing a wild mustang charging up First Avenue, Fogarty took to the chase. Cheered on by hundreds of spectators, he gained on the horse and caught a rope attached to its halter. He was forced to drop the rope at 101st Street in order to save a small boy who stood in their path. According to the story, Fogarty leaned over his bike, picked up the boy by his collar, and carried him out of harm’s way. Without missing a beat, he continued chasing the horse until he caught him again at 106th Street. The horse was taken to the police stables on East 104th Street.
Father of the Police Drama
When he wasn’t saving women, children, and drunken men, Fogarty was busy volunteering as the first drum major and leader of the new Police Band, which he helped organize in 1903. He also wrote police dramas, which were performed for the benefit of the department relief fund.
In 1905, Fogarty wrote an article suggesting that a film be made on the life of a New York City policeman. He was immediately approached by Frederick Freeman Proctor (F.F. Proctor’s Enterprises), a theatre and vaudeville circuit manager. Commissioner William McAdoo liked the idea of including the New York Police in movie scripts, and so paved the way for the myriad of police movies and TV shows.
2585 Marion Avenue in the Fordham section of the Bronx, Fogarty residence
According to the 1920 census, Daniel Fogarty and his wife, Anna, lived in this circa 1901 two-story frame house at 2585 Marion Avenue in the Fordham section of the Bronx with their children Harriet, Harry, Gertrude and Anna. Prior to living here, the family lived on Webster Avenue and then at 375 East 199th Street in the Bronx.
Sergeant Fogarty and Colonel John Jacob Astor IV
In addition to the heroics, Daniel Fogarty was one of the first organizers of the department’s Widows’ and Orphans Relief Fund. As the leader of the Police Band, he thought it would be a good idea for the band to raise money for the wives and families of policemen who were injured or killed in the line of duty.
It was while working with Commissioner McAdoo on this initiative that Fogarty met Colonel John Jacob Astor. Not only did Astor assist in creating the fund, but he also worked with Fogarty to help form the Honor Legion of the Police Department, which was composed of men who rendered distinguished service in time of great danger.
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Vincent Astor
After his father, John Jacob Astor IV, went down with the Titanic, 20-year-old Vincent Astor inherited a massive fortune. The richest boy in the world made headlines when he sold off the family’s slum housing and reinvested in reputable enterprises to help the less fortunate.

When Astor died on the Titanic in 1911, his son Vincent Astor took his place on the fund. Shortly after Sergeant Fogarty retired due to a heart condition in July 1914 (he was then stationed at the East 51st Street Station), Vincent presented him with a $20,000 building on land belonging to the Astor estate at 149th Street and 8th Avenue. Daniel, his wife, Anna, and son Harry opened the Screen Theater – what was then called a “moving picture theater” — in October 1914.
Sergeant Daniel J. Fogarty
The highly decorated Sergeant Daniel J. Fogarty retired in July 1914 due to a heart condition.
By 1920, Daniel Fogarty was fully retired and had turned the theater business over to his son. He died at home in the Bronx on August 13, 1921. By that time, the goats, the squatters, and the shanties were gone, too.
Today, the land once occupied by the thriving Harlem Market, where Policeman Fogarty fought crime and saved lives on his bicycle, is occupied by the East River Houses, a large public housing development completed in 1941. The former 104th Street Station is still standing, only now it’s owned by Hope Community, Inc., a non-profit housing organization founded in 1968 to “develop, revitalize and beautify East Harlem.”