Health News UK

By scienceblog.com

Lung cancer is the deadliest form of cancer in the world, and 80% of death are related to smoking. In addition to tobacco control, effective chemoprevention strategies are therefore needed.

A team of scientists from the University of Geneva (UNIGE), Switzerland, studied a well-known natural product, resveratrol, which is found in grapes and in red wine. While its chemopreventive properties against cancers affecting the digestive tract have been documented by previous studies, resveratrol has so far shown no effect on lung cancers. Thanks to nasal administration, the UNIGE team obtained very promising results in a study conducted in mice and described in the journal Scientific Reports.

“We tried to prevent lung cancer induced by a carcinogen found in cigarette smoke by using resveratrol, an already well-documented molecule, in a mouse model,” explains Muriel Cuendet, Associate Professor in the School of pharmaceutical sciences of the UNIGE Faculty of Science. This 26 week long study contained four groups of mice. The first one, the control, received neither carcinogen nor resveratrol treatment. The second received only the carcinogen, the third received both the carcinogen and the treatment, and the fourth received only the treatment. “We observed a 45% decrease in tumor load per mouse in the treated mice. They developed fewer tumors and of smaller size than untreated mice,” says Muriel Cuendet. When comparing the two groups that were not exposed to carcinogen, 63% of the mice treated did not develop cancer, compared to only 12.5% of the untreated mice. “Resveratrol could therefore play a preventive role against lung cancer,” she continues.

This formulation is applicable to humans
However, resveratrol does not seem suitable for preventing lung cancer: when ingested, it is metabolized and eliminated within minutes, and therefore does not have time to reach the lungs. “This is why our challenge was to find a formulation in which resveratrol could be solubilized in large quantities, even though it is poorly soluble in water, in order to allow nasal administration. This formulation, applicable to humans, allows the compound to reach the lungs,” explains Aymeric Monteillier, a scientist in the School of pharmaceutical sciences of the UNIGE Faculty of Science, and the first author of the study. The resveratrol concentration obtained in the lungs after nasal administration of the formulation was 22 times higher than when taken orally. The chemoprevention mechanism is probably related to apoptosis, a process by which cells program their own death and from which cancer cells escape. The UNIGE research team will now focus on finding a biomarker that could contribute to the selection of people eligible for preventive treatment with resveratrol.

Towards a preventive treatment?
Resveratrol is an already well-known molecule, which is found in food supplements, meaning that no further toxicological study would be needed prior to commercialisation as a preventive treatment. “This discovery is unfortunately of little economic interest to pharmaceutical groups. The molecule is indeed simple and non-patentable and cancer prevention studies require a follow-up over many years,” regrets Muriel Cuendet, without excluding the development of preventive treatment in humans.

By By Kyla Cathey, Earth.com

Red wine may play a role in lung cancer prevention – but not if all you do is drink it.

The chemical compound resveratrol, which is found in grapes, may help protect against lung cancer by reducing cancer-causing cells in the body.

In a new study conducted by scientists at the University of Geneva, the compound reduced cancerous cells in mice and even aided in lung cancer prevention.

But the mice didn’t drink it. Instead, they inhaled it nasally.

The Swiss scientists exposed mice to a cancer-causing chemical in cigarette smoke, then split the mice who developed lung cancer into two groups. One group was given the red wine compound resveratrol for 26 weeks, while the other received no treatment. The scientists also treated mice who had not yet developed tumors with the compound.

Of the mice who had lung cancer at the start of the study, the ones treated with the resveratrol saw their cancerous cells reduced by 45 percent. They had fewer and smaller tumors than the untreated group.

The red wine compound also helped with cancer prevention. In the group of mice that had been exposed to the cigarette chemical and not received any treatment with resveratrol, 87.5 percent went on to develop lung cancer. Only 37 percent of the mice “pre-treated” with the compound went on to develop cancer.

But taken orally, the compound broke down before reaching the lungs.

“This is why our challenge was to find a formulation in which resveratrol could be solubilised in large quantities, even though it is poorly soluble in water, in order to allow nasal administration,” lead author Aymeric Monteillier told the Daily Mail. “This formulation, applicable to humans, allows the compound to reach the lungs.”

The scientists believe that the compound may trigger a process called apoptosis – a sort of “suicide” trigger in cancer cells.

Because resveratrol is already found in red wine and other foods, safety studies aren’t needed before it could be approved for cancer prevention, the scientists said.

The team is now working to develop a test that would help determine if patients are eligible for the preventative treatment.

Resveratrol is a plant polyphenol that has potent anti-inflammatory and anti-oxidant properties. Age-related macular degeneration is a degenerative condition characterized by elevated levels of oxidation triggered cell damage and a subsequent inflammatory cascade. Resveratrol prevents activation of inflammatory pathways and is also a potent scavenger of reactive oxygen species and free radicals. Experiments using the mouse model have demonstrated that resveratrol reduces angiogenesis. The evidence suggests that resveratrol would be a useful inclusion in ocular nutritional supplements.

Download the PDF

Endothelium-dependent nitric oxide–mediated vasodilation is impaired in rats with pulmonary hypertension (PH) induced by chronic hypoxia or by monocrotaline injection. We therefore investigated whether the prolonged administration of the nitric oxide precursor l-arginine would alleviate PH in both rat models.

Methods and Results Fifty-nine rats were exposed to hypobaric hypoxia (380 mm Hg, 10 days) or room air and injected intraperitoneally with l-arginine (500 mg/kg), d-arginine (500 mg/kg), or saline once daily from day −3 to day 10. An additional 38 rats injected subcutaneously with monocrotaline (60 mg/kg) or saline were treated similarly with l-arginine or saline from day −3 to day 17. At the end of the experiment, awake mean pulmonary arterial pressure was determined. The heart was dissected to weigh the right ventricle, and the lungs were obtained for vascular morphometric analysis. Hypoxic rats developed PH (30.8±0.7 versus 19.2±0.4 mm Hg in controls; P<.05) and right ventricular hypertrophy. Their pulmonary arterial wall thickness and the proportion of muscular arteries in the peripheral arteries increased. l-Arginine but not d-arginine reduced PH (24.8±0.7 mm Hg; P<.05), right ventricular hypertrophy, and pulmonary vascular disease. Monocrotaline rats developed PH (34.9±2.1 versus 18.8±1.2 mm Hg in controls; P<.05), right ventricular hypertrophy, and pulmonary vascular disease. Again, l-arginine reduced PH (24.3±1.7 mm Hg; P<.05), right ventricular hypertrophy, and pulmonary vascular disease.

Conclusions We conclude that l-arginine ameliorated the changes associated with PH in rats, perhaps by modifying the endogenous nitric oxide production.

Footnotes
Correspondence to Yoshihide Mitani, MD, Department of Pediatrics, Mie University School of Medicine, 2-174 Edobashi, Tsu City, Mie Pref, Japan 514.
References
1 Meyrick B, Reid L. Endothelial and subintimal changes in rat hilar pulmonary artery during recovery from hypoxia. Lab Invest.1980;42:603-615.MedlineGoogle Scholar
2 Rosenberg H, Rabinovitch M. Endothelial injury and vascular reactivity in monocrotaline pulmonary hypertension. Am J Physiol.1988;255:H1484-H1491.MedlineGoogle Scholar
3 Adnot S, Raffestin B, Eddahibi S, Braquest P, Chabrier PE. Loss of endothelium-dependent relaxant activity in the pulmonary circulation of rats exposed to chronic hypoxia. J Clin Invest.1991;87:155-162.CrossrefMedlineGoogle Scholar
4 Maruyama J, Maruyama K. Impaired nitric oxide-dependent responses and their recovery in hypertensive pulmonary arteries of rats. Am J Physiol.1994;266:H2476-H2488.MedlineGoogle Scholar
5 Altiere RJ, Olson JW, Gillespie MN. Altered pulmonary vascular smooth muscle responsiveness in monocrotaline-induced pulmonary hypertension. J Pharmacol Exp Ther.1986;236:390-395.MedlineGoogle Scholar
6 Rabinovitch M, Bothwell T, Hayakawa BN, Williams WG, Trusler GA, Rowe RD, Olley PM, Cutz E. Pulmonary artery endothelial abnormalities in patients with congenital heart defects and pulmonary hypertension. Lab Invest.1986;55:632-653.MedlineGoogle Scholar
7 Moncada S, Higgs EA. The l-arginine-nitric oxide pathway. N Engl J Med.1993;329:2002-2012.CrossrefMedlineGoogle Scholar
8 Dinh-Xuan AT, Higenbottam TW, Clelland CA, Pepke-Zaba J, Cremona G, Butt AY, Large SR, Wells FC, Wallwork J. Impairment of endothelium-dependent pulmonary-artery relaxation in chronic obstructive lung disease. N Engl J Med.1991;324:1539-1547.CrossrefMedlineGoogle Scholar
9 Celermajer DS, Cullen S, Deanfield JE. Impairment of endothelium-dependent pulmonary artery relaxation in children with congenital heart disease and abnormal pulmonary hemodynamics. Circulation.1993;87:440-446.CrossrefMedlineGoogle Scholar
10 Pepke-Zaba J, Higenbottam TW, Dinh-Xuan AT, Stone D, Wallwork J. Inhaled nitric oxide as a cause of selective pulmonary vasodilation in pulmonary hypertension. Lancet.1992;388:1173-1174.Google Scholar
11 Frostell C, Fratacci MD, Wain JC, Jones R, Zapol WM. Inhaled nitric oxide, a selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction. Circulation.1992;83:2038-2047.Google Scholar
12 Kouyoumdjian C, Adnot S, Levame M, Eddahibi S, Bousbaa H, Raffestin B. Continuous inhalation of nitric oxide protects against development of pulmonary hypertension in chronically hypoxic rats. J Clin Invest.1994;94:578-584.CrossrefMedlineGoogle Scholar
13 Roberts JD, Roberts CT, Jones RC, Zapol WM, Bloch KD. Continuous nitric oxide inhalation reduces pulmonary arterial structural changes, right ventricular hypertrophy, and growth retardation in the hypoxic newborn rat. Circ Res.1995;76:215-222.CrossrefMedlineGoogle Scholar
14 Mehta S, Stewart DJ, Langleben D, Levy RD. Short-term pulmonary vasodilation with l-arginine in pulmonary hypertension. Circulation.1995;92:1539-1545.CrossrefMedlineGoogle Scholar
15 Ilkiw R, Todorovich-Hunter L, Maruyama K, Shin J, Rabinovitch M. SC-39026, a serine elastase inhibitor, prevents muscularization of peripheral arteries, suggesting a mechanism of monocrotaline-induced pulmonary hypertension in rats. Circ Res.1989;64:814-825.CrossrefMedlineGoogle Scholar
16 Maruyama K, Ye C, Woo M, Venkatacharya H, Lines LD, Silver MM, Rabinovitch M. Chronic hypoxic pulmonary hypertension in rats and increased elastolytic activity. Am J Physiol.1991;261:H1716-H1726.MedlineGoogle Scholar
17 Rabinovitch M, Konstam MA, Gamble WJ, Papanicolaou N, Aronovitz MJ, Treves S, Reid L. Changes in pulmonary blood flow affect vascular response to chronic hypoxia in rats. Circ Res.1983;52:432-441.CrossrefMedlineGoogle Scholar
18 Meyrick B, Reid L. The effect of continued hypoxia on rat pulmonary arterial circulation: an ultrastructural study. Lab Invest.1978;38:188-200.MedlineGoogle Scholar
19 Hislop A, Reid L. New findings in pulmonary arteries of rats with hypoxia-induced pulmonary hypertension. Br J Exp Pathol.1976;57:542-554.MedlineGoogle Scholar
20 Grover RF, Johnson RL, McCullough RG, McCullough RE, Hofmeister SE, Campbell WB, Reynolds RC. Pulmonary hypertension and pulmonary vascular reactivity in beagles at high altitude. J Appl Physiol.1988;65:2632-2640.CrossrefMedlineGoogle Scholar
21 Wagenvoort CA, Wagenvoort N. Hypoxic pulmonary vascular lesions in man at high altitude and in patients with chronic respiratory disease. Pathol Microbiol (Basel).1973;39:276-282.MedlineGoogle Scholar
22 Eddahibi S, Adnot S, Carville C, Blouquit Y, Raffestin B. l-Arginine restores endothelium-dependent relaxation in pulmonary circulation of chronically hypoxic rats. Am J Physiol.1992;263:L194-L200.CrossrefMedlineGoogle Scholar
23 Cooke JP, Singer AH, Tsao P, Zera P, Rowan RA, Billingham ME. Antiatherogenic effects of l-arginine in the hypercholesterolemic rabbit. J Clin Invest.1992;90:1168-1172.CrossrefMedlineGoogle Scholar
24 Hamon M, Vallet B, Bauter C, Wernert N, McFadden EP, Lablanche J, Dupuis B, Bertrand ME. Long-term oral administration of l-arginine reduces intimal thickening and enhances neoendothelium-dependent acetylcholine-induced relaxation after arterial injury. Circulation.1994;90:1357-1362.CrossrefMedlineGoogle Scholar
25 Chen PY, Sanders PW. l-Arginine abrogates salt-sensitive hypertension in Dahl/Rapp rats. J Clin Invest.1991;88:1559-1567.CrossrefMedlineGoogle Scholar
26 Gallego MJ, Farre AL, Riesco A, Monton M, Granders SM, Barat A, Hernando L, Casado S, Caramelo CA. Blockade of endothelium-dependent responses in conscious rats by cyclosporin A: effect of l-arginine . Am J Physiol.1993;264:H708-H714.MedlineGoogle Scholar
27 Gold ME, Bush PA, Ignarro LJ. Depletion of arterial l-arginine causes reversible tolerance to endothelium-dependent relaxation. Biochem Biophys Res Commun.1989;164:714-721.CrossrefMedlineGoogle Scholar
28 Gold ME, Wood KS, Buga GM, Byrns RE, Ignarro LJ. l-Arginine causes whereas L-argininosuccinic acid inhibits endothelium-dependent vascular smooth muscle relaxation. Biochem Biophys Res Commun.1989;161:536-543.CrossrefMedlineGoogle Scholar
29 Palmer RM, Rees DD, Ashton DS, Moncada S. l-Arginine is the physiological precursor for the formation of nitric oxide in endothelium-dependent relaxation. Biochem Biophys Res Commun.1988;153:1252-1256.Google Scholar
30 Zhau L, Crawley DE, Hughes JM, Evans TW, Winter RJ. Endothelium-derived relaxing factor activity in rat lung during hypoxic pulmonary vascular remodeling. J Appl Physiol.1993;74:1061-1065.CrossrefMedlineGoogle Scholar
31 Hampl V, Archer SL, Nelson DP, Weir EK. Chronic EDRF inhibition and hypoxia: effects on pulmonary circulation and systemic blood pressure. J Appl Physiol.1993;75:1748-1757.CrossrefMedlineGoogle Scholar
32 Dinh-Xuan AT, Pepke-Zaba J, Higenbottam TW. Impairment of nitric oxide production in isolated pulmonary arteries of patients with chronic hypoxic pulmonary hypertension: putative mechanisms and pathophysiological implications. In: Moncada S, Marletta MA, Higgs JB Jr, Higgs EA, eds. The Biology of Nitric Oxide: 1.Physiological and Clinical Aspects. London, UK: Portland Press; 1992:381-384.Google Scholar
33 Carville C, Eddahibi S, Adnot S, Raffestin B. In vivo but not in vitro administration of l-arginine restores EDRF activity in pulmonary arteries from chronically hypoxic rats. FASEB J.1992;6:A1168. Abstract.Google Scholar
34 Kourembanas S, McQuillan LP, Leung GK, Faller DV. Nitric oxide regulates the expression of vasoconstrictors and growth factors by vascular endothelium under both normoxia and hypoxia. J Clin Invest.1993;92:99-104.CrossrefMedlineGoogle Scholar
35 Eddahibi S, Raffestin B, Clozel M, Levame M, Adnot S. Protection from pulmonary hypertension with an orally active endothelin receptor antagonist in hypoxic rats. Am J Physiol.1995;268:H828-H835.MedlineGoogle Scholar
36 Katayose D, Ohe M, Yamauchi K, Ogata M, Shirato K, Fujita H, Shibahara S, Takishima T. Increased expression of PDGF A- and B-chain genes in rat lungs with hypoxic pulmonary hypertension. Am J Physiol.1993;264:L100-L106.MedlineGoogle Scholar
37 Maruyama J, Maruyama K, Mitani Y, Kitabatake M, Yamauchi T, Miyasaka K. Continuous low-dose NO inhalation does not prevent monocrotaline-induced pulmonary hypertension in rats. Am J Physiol.1997;272:H517-H524.MedlineGoogle Scholar
38 Ono S, Voelkel NF. PAF antagonists inhibit monocrotaline-induced lung injury and pulmonary hypertension. J Appl Physiol.1991;71:2483-2492.CrossrefMedlineGoogle Scholar
39 Carillo L, Aviado DM. MCT-induced pulmonary hypertension and p-chlorophenylalanine. Lab Invest.1969;20:243-248.MedlineGoogle Scholar
40 Voelkel NF, Tuder RM, Bridge J, Arend WP. Interleukin-1 receptor antagonist treatment reduces pulmonary hypertension generated in rats by monocrotaline. Am J Respir Cell Mol Biol.1994;11:664-675.CrossrefMedlineGoogle Scholar
41 Meyrick B, Gamble W, Reid L. Development of Crotalaria pulmonary hypertension: hemodynamic and structural study. Am J Physiol.1980;239:H692-H702.CrossrefMedlineGoogle Scholar
42 Adams MR, Forsyth CJ, Jessup W, Robinson J, Celermajer DS. Oral l-arginine inhibits platelet aggregation but does not enhance endothelium-dependent dilation in healthy young men. J Am Coll Cardiol.1995;26:1054-1061.CrossrefMedlineGoogle Scholar
43 Caterina RD, Libby P, Peng H, Thannickak VJ, Rajavashisth TB, Gimbrone MA, Shin WS, Liao JK. Nitric oxide decreases cytokine-induced endothelial activation: nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. J Clin Invest.1995;96:60-68.CrossrefMedlineGoogle Scholar
44 Tsao PS, McEvoy LM, Drexler H, Butcher EC, Cooke JP. Enhanced endothelial adhesiveness in hypercholesterolemia is attenuated by l-arginine. Circulation.1994;89:2176-2182.CrossrefMedlineGoogle Scholar
45 Clancy R, Leszczynska-Piziak J, Abramson S. Nitric oxide, an endothelial cell relaxation factor, inhibits neutrophil superoxide anion production via a direct action on the NADPH oxidase. J Clin Invest.1992;90:1116-1121.CrossrefMedlineGoogle Scholar
46 Huie RE, Padmaja S. Reaction of NO with superoxide. Free Radic Res Commun.1993;18:195-199.CrossrefMedlineGoogle Scholar
47 Carp H, Janoff A. In vivo suppression of serum elastase-inhibitory capacity by reactive oxygen species generated by phagocytosing polymorphonuclear leukocytes. J Clin Invest.1979;63:793-797.CrossrefMedlineGoogle Scholar
48 Lo YYC, Cruz TF. Involvement of reactive oxygen species in cytokine and growth factor induction of c-fos expression in chondrocytes. J Biol Chem.1995;270:11727-11730.CrossrefMedlineGoogle Scholar
49 Lonn EM, Yusuf S, Jha P, Montague TJ, Teo KK, Benedict CR, Pitt B. Emerging role of angiotensin-converting enzyme inhibitors in cardiac and vascular protection. Circulation.1994;90:2056-2069.CrossrefMedlineGoogle Scholar
50 Williams JK, Adams MR, Herrington DM, Clarkson TB. Short-term administration of estrogen and vascular responses of atherosclerotic coronary arteries. J Am Coll Cardiol.1992;20:452-457.CrossrefMedlineGoogle Scholar
51 Shimokawa H, Lam JYT, Chesebro JH, Bowie EJW, Vanhoutte PM. Effects of dietary supplementation with cod-liver oil on endothelium-dependent responses in porcine coronary arteries. Circulation.1987;76:898-905.CrossrefMedlineGoogle Scholar

By STEPHEN MATTHEWS ASSISTANT HEALTH EDITOR FOR MAILONLINE

Millions of arthritis patients may enjoy relief by taking a super dose of the antioxidant.

A powerful compound abundant in red wine could help millions of osteoarthritis patients battle their daily agony.

Researchers found patients with painful knee joints given resveratrol – found in the skin of red grapes - reported much less pain.

They also had much lower levels of inflammation in their knees, according to the Iraqi scientists behind the study.

Eight million people in the UK and 54 million in the US suffer from osteoarthritis - when the cartilage gradually becomes thin.

It is different to rheumatoid arthritis, a long-term illness in which the immune system causes the body to attack itself.

Despite not being caused by inflammation, patients with osteoarthritis can still have inflamed areas when their cartilage breaks down.

Scientists at the Al-Rafidain University College in Baghdad led the new three-month study of 110 patients.

Half were given a 500mg daily dose of resveratrol alongside 15mg of meloxicam – a drug used to treat pain and inflammation. The others were instead given a placebo.

Blood tests were taken before and after the study to examine levels of inflammatory biomarkers.

Results showed patients given an oral resveratrol supplement had a much lower pain score, compared to their placebo-taking peers.

They also had ‘significantly’ lower levels of blood biomarkers of inflammation common in those battling knee osteoarthritis.

The study also involved scientists at the Shar Teaching Hospital in Kurdistan and was published in the Journal of Medicinal Food.

Resveratrol - an antioxidant also found in peanuts - has been proven to have anti-inflammatory properties in an array of studies.

It has also been found to cut harmful cholesterol, protect brain function and lower blood pressure.

However, much of the research on resveratrol has been done in animals and test tubes using high amounts of the compound.

Most human studies have focused on supplemental forms of the compound, in super-strength concentrations higher than that found in wine.

The average glass of red wine contains 2mg of resveratrol, according to the Linus Pauling Institute at Oregon State University.

This means people would need to consume 250 glasses of red wine each day – which would be deadly - to achieve the 500mg used in the study.

Arthritis Research UK said it would be interested to see more research to understand how resveratrol could benefit people in the long term.

Resveratrol is a naturally occurring polyphenol that provides several health benefits including cardioprotection and cancer prevention. However, its biological activity is limited by a poor bioavailability when taken orally. The aim of this work was to evaluate the capability of casein nanoparticles as oral carriers for resveratrol. Nanoparticles were prepared by a coacervation process, purified and dried by spray-drying. The mean size of nanoparticles was around 200 nm with a resveratrol payload close to 30 g/mg nanoparticle. In vitro studies demonstrated that the resveratrol release from casein nanoparticles was not affected by the pH conditions and followed a zero-order kinetic. When nanoparticles were administered orally to rats, they remained within the gut, displaying an important capability to reach the intestinal epithelium. No evidence of nanoparticle “translocation” were observed. The resveratrol plasma levels were high and sustained for at least 8 h with a similar profile to that observed for the presence of the major metabolite in plasma. The oral bioavailability of resveratrol when loaded in casein nanoparticles was calculated to be 26.5%, 10 times higher than when the polyphenol was administered as oral solution. Finally, a good correlation between in vitro and in vivo data was observed.

Download the PDF

By HospiMedica International staff writers

Administration of nitric oxide (NO) during and following heart surgery can decrease risk of developing acute and chronic kidney problems, claims a new study.

Researchers at Fourth Military Medical University (Xi’an, China), Brigham and Women’s Hospital (BWH; Boston, MA, USA), Massachusetts General Hospital (MGH; Boston, USA), and other institutions conducted a randomized, controlled trial involving 244 adults in Xi'an (China), who underwent multiple valve replacement surgery. The patients were randomized to receive 80 PPM of NO or of nitrogen alone, administered via a gas exchanger during cardiopulmonary bypass, and by inhalation for 24 hours post-operatively.

The results revealed that patients who received of NO during and for 24 hours after surgery were less likely to develop acute kidney injury (AKI), with a decrease from 64% in placebo-treated patients to 50% in those who received NO. Risk of progressing to stage 3 chronic kidney disease (CKD) was also reduced at 90 days, from 33% in placebo-treated patients to 21% in those who received NO. After one year, 31% of patients in the nitrogen placebo group had serious kidney disease, compared to 18% in the NO group. There was also a decrease in the overall one-year mortality rate, from 6% in the placebo group to 3% in the NO group. The study was published on June 22, 2018, in Journal of Respiratory and Critical Care Medicine.

“We tested whether administration of nitric oxide, a gas normally produced by cells in the lining of blood vessels, might render hemoglobin ‘inert’, thereby decreasing the risk of both acute and chronic kidney injury,” said co-lead author Lorenzo Berra, MD, medical director of respiratory care at MGH. “We believe that the older patients with an increased number of cardiovascular risk factors, including obesity, hypertension, and diabetes, may derive even greater benefit from nitric oxide administration during and after heart surgery.”

NO has been identified as an important molecule with versatile roles in human physiology, including selective pulmonary vasodilation, bronchodilator, and pulmonary surfactant activities to improve ventilation-perfusion mismatch and hence oxygenation. Clinical effects of nitric oxide gas include cardio-pulmonary vasodilation, reduction of right heart load, reduction of ischemia, reduction of hypoxemia, inhibition of platelet aggregation, and anti-inflammatory, fungicidal, virocidal, and bactericidal effects, among others.

By HospiMedica International staff writers

Women who are unable to quit smoking during their pregnancy may reduce the harm smoking does to their baby's lungs by taking vitamin C, according to a new study.

Researchers at Oregon Health & Science University (OHSU; Portland, USA), the Indiana University School of Medicine (Indianapolis, USA), and other institutions conducted a randomized, double-blind, placebo-controlled trial to evaluate pulmonary function at three months of age in infants delivered to pregnant smokers, in order to see if Vitamin C could decrease the effects of smoking during pregnancy on infant lung function. To do so, they measured force expiratory flows (FEFs) at three and 12 months of babies born to 252 mothers who smoked. On average, the mothers in both arms of the study who could not quit smoked seven cigarettes a day.

The mothers who smoked were randomized between 13 and 23 weeks gestation to either 500 mg of supplemental vitamin C every day or a placebo, in addition to the same prenatal vitamin. FEFs were measured at three intervals, and defined by the percentage of air remaining in the lung during forced exhalation: FEF75, FEF25-75, and FEF50. The results showed a statistically significant difference in lung function between the babies born to the two groups at the FEF25-75 and FEF50 intervals at three months.

And at 12 months, a statistically significant difference in lung function was identified between the two groups at all three intervals. The study also found that babies whose mothers took vitamin C were less likely to develop wheeze at one year. The study did not find a significant difference between the two groups of babies in gestational age at delivery, delivery mode, incidence of prematurity, or birth weight. The study was presented at the annual American Thoracic Society (ATS) conference, held during May 2018, in San Diego (CA, USA).

“We performed FEFs in this study because they provide a more direct measurement of actual air way function, and are more predictive of future disease,” said lead author professor of pediatrics Cynthia McEvoy, MD, of the OHSU Doernbecher Children's Hospital. “Getting women to quit smoking during pregnancy has to be priority one. For those roughly 50% of pregnant smokers who will not, or cannot quit despite all efforts, quit smoking, vitamin C supplementation may be a simple and safe way to help their babies breathe better.”

Smoking during pregnancy is the largest preventable cause of childhood respiratory illness, including decreased pulmonary function, wheezing, and asthma. Despite strong anti-smoking efforts, at least 12% of American women cannot quit smoking when pregnant, resulting in over 450,000 smoke-exposed infants born yearly. Preliminary data suggests that the mechanism underlying vitamin C’s prevention of some of the effects of maternal smoking on offspring pulmonary health involves the prevention of epigenetic changes induced by maternal smoking.

Source: HospiMedica International

By HospiMedica International staff writers

Higher levels of serum 25-hydroxyvitamin D [25(OH)D] are associated with a significant decreased risk of breast cancer, according to a new study.

Researchers at the University of California, San Diego (UCSD, USA), GrassrootsHealth (Encinitas, CA, USA), and other institutions conducted an epidemiological study that pooled data from two randomized clinical trials for a total of 5,038 participants (average age 63 years) in order to examine the association between risk of female breast cancer and a broad range of 25(OH)D concentrations, the main form of vitamin D in blood. All participants were free of cancer at enrollment and were followed for a mean period of four years.

The results showed 77 women were diagnosed with breast cancer. There was an 82% lower incidence rate of breast cancer for women with 25(OH)D concentrations higher that ng/ml ≥60, compared to those with concentrations lower than 20 ng/ml, with the highest proportion of breast cancer-free women in the 60 ng/ml and higher group (99.3%). Analysis revealed that after adjustment, women with 25(OH)D concentrations that were higher than 60 ng/ml had an 80% lower risk of breast cancer than those with concentrations lower than 20 ng/ml. The study was published on June 15, 2018, in PLOS One.

“To reach 25(OH)D levels of 60 ng/ml would generally require dietary supplements of 4,000 to 6,000 international units per day, less with the addition of moderate daily sun exposure wearing very minimal clothing,” said study co- author Professor Cedric Garland, PhD, of UCSD, who added that “the success of oral supplementation should be determined using a blood test, preferably during winter months.”

Vitamin D is a group of fat-soluble secosteroids found in many dietary sources, such as fish, eggs, fortified milk, and cod liver oil, which can also be synthesized in adequate amounts by all mammals from sunlight. Current recommended average daily amounts are 400 IU for children up to one year; 600 IU for ages one to 70 years (including pregnant or breastfeeding women), and 800 IU for persons over age 70, according to the U.S. National Academy of Medicine.

Source: HospiMedica International

By HospiMedica International staff writers

Circulating nitric oxide (NO) can help cardiac drugs improve heart function, but deficiencies could exacerbate heart failure (HF), according to a new study.

Researchers at Case Western Reserve University (CWRU; Cleveland, OH, USA), Duke University (Durham NC, USA), and other institutions conducted a study in mice that focused on one of the most common drug targets in modern medicine, the G protein-coupled receptor (GPCR). When drugs like beta-blockers attach to GPCRs, they influence protein pathways inside the cells. One pathway activates therapeutic G proteins, while a second pathway activates arrestins that can lead to side effects. NO is known to have an established role in receiving signals from GPCRs.

The researchers therefore genetically engineered mice to lack the ability to attach NO to one half of the pathway, the arrestin proteins that can trigger side effects; they found that without NO signaling, the mice could not increase heart rate or pump function. The results suggest HF severity could vary based on NO levels in the body. Low NO levels could cause GPCRs to primarily activate the β-arrestin side of the signaling pathways, excluding the other half that helps the heart respond to stressors.

The researchers confirmed their findings in human tissue samples, collected from hearts involved in transplants. In nearly two-thirds of failing heart samples, the researchers found that NO determined the signaling balance to the β-arrestin pathway. The researchers suggest that with hundreds of GPCRs in the body, managing NO correctly could help existing drugs of all types work with fewer side effects. The study was published on May 3, 2018, in Molecular Cell.

“We have identified a main function of nitric oxide in cellular systems. It likely regulates GPCR signaling across virtually all cell types and tissues. This may bear directly on numerous diseases, as well as the predicted response to therapeutic agents,” said senior author Professor Jonathan Stamler, MD, of CWRU. “Drugs and hormones inevitably regulate both pathways, but if one could shut down the pathway producing side effects, drugs would work better. It is able to use nitric oxide to shut down arrestin-based pathways causing side effects.”

NO has been identified as an important molecule with versatile roles in human physiology, including selective pulmonary vasodilation, bronchodilator, and pulmonary surfactant activities to improve ventilation-perfusion mismatch and hence oxygenation. The clinical effects of NO gas that have been reported include cardio-pulmonary vasodilation, reduction of right heart load, reduction of ischemia, reduction of hypoxemia, inhibition of platelet aggregation, and anti-inflammatory, fungicidal, virocidal, and bactericidal effects, among others.

Source: HospiMedica International

Pages

 


Salutem Supplements Ltd
27 Old Gloucester Street
London
WC1N 3AX
United Kingdom
Customer Services:
+44 202 296438

Terms & Conditions | Privacy Policy

 

Follow Us

 
Zircon - This is a contributing Drupal Theme
Design by WeebPal.