While hospital buildings are often smoke-free, a new study finds that by February 2008, 45 percent of US hospitals had adopted “smoke-free campus” policies, meaning that all the property owned or leased by the hospital, both indoors and outdoors, was smoke-free and there were no designated smoking areas on those properties.

The study, “The Adoption of Smoke-Free Hospital Campuses in the United States,” is the first of its kind to examine the national prevalence of smoke-free hospital campus policies. It was conducted by The Joint Commission, the world’s largest healthcare standards setting and accrediting body, and researchers from the Henry Ford Health System’s Center for Health Promotion and Disease Prevention. The study was funded by the Substance Abuse Policy Research Program of the Robert Wood Johnson Foundation and appears in the online version of the peer-reviewed journal Tobacco Control.

“Besides the 45 percent that already had smoke-free campuses, another 15 percent indicated that they would be implementing similar policies in the near future. Hence, it is safe to assume on the basis of these results that the majority of US hospitals will have smoke-free campuses by the end of 2009,” according to Scott C. Williams, PsyD, of The Joint Commission.

The 2008 data shows that not-for-profit hospitals were more likely to have smoke-free campuses than for-profit hospitals. The 2008 data also shows that hospitals in Arkansas, Iowa, Massachusetts, Minnesota, Oklahoma and Wisconsin had among the highest proportion of smoke-free campuses. Hospitals in several tobacco states also had significant proportion of smoke-free campuses.

“In 1992, The Joint Commission implemented a standard which required hospitals to adopt a non-smoking policy throughout all buildings, limiting smoking to separate, ventilated areas. At that time, fewer than 3 percent of hospitals extended this indoor smoking ban to include the entire hospital campus, both indoors and outdoors. Our study shows that around 2004-2005 this began to change dramatically. Now a majority of the nation’s hospitals do not allow smoking anywhere on their property,” Williams said.

The study examined the current smoking policies and future plans of 1,916 Joint Commission-accredited hospitals to determine the prevalence of smoke-free hospital campus policies and whether such policies had an impact on smoking cessation counseling offered in those hospitals. The study found that not-for-profit hospitals were slightly more likely to offer smoking cessation counseling than for-profit hospitals.

The study also found that federally owned hospitals were less likely to have smoke-free campuses. This, according to the study, was likely due to the influence of federal legislation requiring all Veterans Administration (VA) hospitals to have a suitable and accessible patient indoor smoking area for patients and residents. “Such legislation makes it virtually impossible for VA hospitals to adopt a completely smoke-free campus,” Williams said.

The Substance Abuse Policy Research Program (saprp) of the Robert Wood Johnson Foundation funds research into policies related to alcohol, tobacco and illegal drugs.

Source:
Carol Vieira

Burness Communications

Prabhu Ponkshe

Substance Abuse Policy Research Program

Men with signs of benign prostatic hyperplasia (BPH) can be helped with a daily dose of tadalafil (Cxxxxs®) to relieve associated lower urinary tract symptoms (LUTS), according to a new study published in the October 2008 issue of The Journal of Urology. Researchers from the University of Texas Southwestern Medical Center at Dallas, Northwestern University and Lilly Research Laboratories report on a randomized, double-blind, placebo-controlled study of over 1000 men in ten countries.

Claus G. Roehrborn, MD, Professor of Urology, University of Texas Southwestern Medical Center, states, “Since reports of [impotence] incidence, pathophysiology and treatment have shown a possible link between BPH LUTS and [impotence]. PDE5 inhibitors like tadalafil (Cxxxxx®) have received increased attention for treating BPH LUTS, although they are currently only approved for [impotence]. The half-life of tadalafil is 17.5 hours, making it suitable as once daily therapy. Although the precise mechanism of action by which PDE5 inhibitors may alleviate LUTS is not completely understood, several putative mechanisms are currently under investigation.”

Men with signs of BPH may experience LUTS, such as urinary frequency, urgency, intermittence, nocturia, straining, incomplete emptying or a weak urinary stream. LUTS increase with age with an overall prevalence of greater than 50% in men 50 years or older. Drugs currently used to treat these symptoms can produce unwanted side effects, including dizziness, low blood pressure and sexual dysfunction.

Participants in the tadalafil study were required to have at least a 6-month history of LUTS secondary to BPH. Subjects with a high PSA (more than 10 ng/ml) were excluded, as were subjects with other complicating conditions or conflicting drug treatments. Anyone who had undergone treatment for [impotence] or other BPH treatments underwent a 4-week treatment-free screening period. All participants then received placebo for 4 weeks prior to randomization. The 1056 subjects were then divided randomly into 5 groups that received a placebo, or doses of 2.5, 5.0, 10.0 or 20.0 mg/day of tadalafil.

Using the International Prostate Symptom Score (I-PSS), a validated seven-item questionnaire about LUTS occurring within the last month, the researchers found that all doses of tadalafil were superior to placebo for relieving LUTS, with statistically significant effects at 4, 8 and 12 weeks. The treatments decreased I-PSS scores from 3.9 to 5.2 points in the different dosage groups, a clinically meaningful improvement according to the guidelines of the American Urological Association. Of the doses studied, 5 mg per day improved the I-PSS by 4.9 points and provided the best risk-benefit profile.

The article is “Tadalafil Administered Once Daily for Lower Urinary Tract Symptoms Secondary to Benign Prostatic Hyperplasia: A Dose Finding Study” by Claus G. Roehrborn, Kevin T. McVary, Albert Elion-Mboussa and Lars Viktrup. It appears in The Journal of Urology, Volume 180, Issue 4 (October 2008) published by Elsevier.

About The Journal Of Urology®

Established in 1917, The Journal of Urology is the official journal of the American Urological Association. It is the most widely read and highly cited journal in the field. It brings to its readership all the clinically relevant information needed to stay at the forefront of this dynamic field. This top-ranking journal presents investigative studies on critical areas of research and practice, survey articles providing short condensations of the best and most important urology literature worldwide and practice-oriented reports on interesting clinical observations.

About Elsevier

Elsevier is a world-leading publisher of scientific, technical and medical information products and services. Working in partnership with the global science and health communities, Elsevier’s 7000 employees in over 70 offices worldwide publish more than 2000 journals and 1900 new books per year, in addition to offering a suite of innovative electronic products, such as ScienceDirect, MD Consult, Scopus, bibliographic databases, and online reference works.

Elsevier is a global business headquartered in Amsterdam, The Netherlands and has offices worldwide. Elsevier is part of Reed Elsevier Group plc, a world-leading publisher and information provider. Operating in the science and medical, legal, education and business-to-business sectors, Reed Elsevier provides high-quality and flexible information solutions to users, with increasing emphasis on the Internet as a means of delivery. Reed Elsevier’s ticker symbols are REN (Euronext Amsterdam), REL (London Stock Exchange), RUK, and ENL (New York Stock Exchange).

Elsevier

An article published Online First and in an upcoming edition of The Lancet reports that new research based on a meta-analysis of thirteen statin trials has shown that use of statins increases the risk of developing type 2 diabetes by 9 percent. Still, the absolute risk is low, especially when compared with the beneficial effect that statins have on reducing coronary events. The article is the work of Professor Naveed Satar and Dr David Preiss, Glasgow Cardiovascular Research Centre, University of Glasgow, UK, and colleagues.

Trials of statin therapy on the risk of development of diabetes in patients given statins have had inconsistent findings. To eliminate this doubt, the authors did a meta-analysis of published and unpublished data in order to find out whether any relation exists between statin use and development of diabetes.

Thirteen trials from the period 1994 to 2009 were included. Each trial had more than 1,000 patients, with identical follow-up in both the statin and non-statin groups and duration of more than one year. Trials of patients with organ transplants, or who needed haemodialysis, were excluded. The thirteen statin trials identified contained a total of 91,140 participants. Of these, 4,278 developed diabetes over an average of four years. A total of 2,226 were assigned statins and 2,052 were assigned control therapy. Statin therapy was associated with a 9 percent increased risk for developing diabetes. There was general consistency in risk across the different trials. Additional analysis showed that the risk of development of diabetes with statins was higher in trials with older participants. On the other hand, baseline body-mass index and change in LDL (bad) cholesterol concentrations did not appear to influence the statin-associated risk of developing diabetes. Treatment of 255 patients with statins for four years resulted in one extra case of diabetes.

The researchers highlight that the findings do not prove that statin therapy raises diabetes risk via a direct molecular mechanism. However, the possibility should be considered. On the other hand, the increased risk could be in some way linked to statin therapy. A slight improvement of survival on statins does not compensate for the increased risk of developing diabetes. Although the authors find it doubtful, they say the increased diabetes risk in those given statins could be a chance finding.

In perspective, treatment of 255 patients with statins for four years would result in one extra case of diabetes. However, for 1 mmol/L reduction in LDL (bad) cholesterol concentrations that statins would cause, the same 255 patients could expect to experience five less major coronary events such as coronary heart disease death or non-fatal heart attack.

The authors advise that monitoring older people receiving statin therapy for development of diabetes could be beneficial since they seem to be more at risk. They explain: “We recommend that development of diabetes is specified as a secondary endpoint in future large endpoint statin trials, and suggest that, when possible, reports of long-term follow-up in existing trials should also include incident diabetes.”

They write in conclusion: “In view of the overwhelming benefit of statins for reduction of cardiovascular events, the small absolute risk for development of diabetes is outweighed by cardiovascular benefit in the short and medium term in individuals for whom statin therapy is recommended. We therefore suggest that clinical practice for statin therapy does not need to change for patients with moderate or high cardiovascular risk or existing cardiovascular disease. However, the potentially raised diabetes risk should be taken into account if statin therapy is considered for patients at low cardiovascular risk or patient groups in which cardiovascular benefit has not been proven.”

In an associated note, Dr Christopher P Cannon, Cardiovascular Division, Brigham and Women’s Hospital and Harvard Medical School, Boston; and TIMI Study Office, Boston, MA, USA, comments on the study. He discusses how the authors of this study projected that 5•4 deaths or heart attacks would be avoided over those four years. Also, nearly the same number of strokes or coronary revascularisation procedures would also be avoided. Dr Cannon remarks: “Thus the benefit [of taking statins] in preventing total vascular events to the risk of diabetes is a ratio of about 9:1 in favour of the cardiovascular benefit. Thus the benefit seems to greatly outweigh the risk.”

He say in closing: “Nonetheless, this newly identified risk does warrant monitoring, and as such, in addition to periodic monitoring of liver-function tests and creatine kinase, it seems reasonable to add glucose to the list of tests to monitor in older patients on statins. Thus, whilst a new risk of statins has been identified, the risk seems small and far outweighed by the benefits of this life-saving class of drugs.”

“Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials”
Naveed Sattar, David Preiss, Heather M Murray, Paul Welsh, Brendan M Buckley, Anton J M de Craen, Sreenivasa Rao Kondapally Seshasai,
John J McMurray, Dilys J Freeman, J Wouter Jukema, Peter W Macfarlane, Chris J Packard, David J Stott, Rudi G Westendorp, James Shepherd,
Barry R Davis, Sara L Pressel, Roberto Marchioli, Rosa Maria Marfisi, Aldo P Maggioni, Luigi Tavazzi, Gianni Tognoni, John Kjekshus, Terje R Pedersen,
Thomas J Cook, Antonio M Gotto, Michael B Clearfield, John R Downs, Haruo Nakamura, Yasuo Ohashi, Kyoichi Mizuno, Kausik K Ray, Ian Ford
DOI: 10.1016/S0140-6736(09)61965-6
The Lancet

Stephanie Brunner (B.A.)

Quality Associates, Inc. (QAI), an established provider of services and solutions for large-scale document management, imaging, and archiving, announced the launch of its H1N1 Flu Vaccine Forms Processing Service, a comprehensive approach to help states, cities, counties, and providers in the private sector successfully and accurately capture and record essential demographic and health data from medical consent forms – a critical step in the administration of the H1N1 vaccine to millions nationwide beginning this fall.

As part of the two-step inoculation process, each patient is required to fill out a printed medical consent form before each shot is given. More than 100 million vaccinations are expected to become available this fall, which is creating a serious and urgent need for states, municipalities and the private sector to immediately develop a clear strategy to effectively capture vital personal and healthcare-related information. Once information is collected, it must be converted into a useable electronic format for insurance, reporting, and statistical needs. Without a digital capture methodology in place, municipalities and private healthcare providers risk losing funds due to lost or inaccurate recipient insurance information. Additionally, government agencies such as the Centers for Disease Control and Prevention could lose important data regarding vaccine distribution and efficacy.

QAI’s H1N1 Flu Vaccine Forms Processing Service involves several steps that ensure information is captured and recorded accurately:

- Step 1 – Consultation: QAI works closely with vaccine administrators to understand the scope of each project, and then helps guide the entire process.

- Step 2 – Forms Design: Using experience gained by processing millions of healthcare forms collected during the administration of the yearly flu vaccine, QAI designs user-friendly forms that collect information as completely and accurately as possible.

- Step 3 – Forms Processing: QAI uses state-of-the-art high-volume scanners, intelligent data recognition software, and technology to capture information on each form. Quality assurance steps ensure the accuracy of all captured data. Additionally, QAI’s controlled, on-shore processing protects sensitive patient information.

- Step 4 – Data Integration: QAI submits all original documentation and captured data back to the client. Data can be provided in one of several formats to ensure compatibility with the provider’s own systems.

Scott Swidersky, director, Information Systems, Quality Associates, Inc., said, “At this moment, every state, local government, and private firm involved in the H1N1 vaccine administration is facing numerous, complex logistical and technical hurdles that must be resolved quickly. In a matter of weeks, the H1N1 vaccine will become available and administration will begin. From a data capture standpoint, QAI is in the unique position of having the vast experience required to successfully pull information from millions of hard-copy documents. We have processed millions of forms used in the administration of yearly flu programs, and are ready to lend our expertise to help in the nationwide H1N1 vaccine administration effort.”

Source
Quality Associates, Inc.

The National Institute for Health and Clinical Excellence (NICE)
has released a positive Final Appraisal Document (FAD) in support of the use of Mimpara®
(cinacalcet) for the treatment of severe secondary hyperparathyroidism (SHPT), a serious
complication of kidney failure, in patients with end stage renal disease (ESRD) on
maintenance dialysis therapy.

SHPT is a common complication of ESRD, where the parathyroid hormone (PTH), which
controls calcium and phosphorus metabolism, is over-produced. Although SHPT can start
without any symptoms, it can slowly cause significant damage to the bones, heart and blood
vessels and if left untreated is associated with an increased risk of hospitalisation, surgery
and mortality.1-5 The number of patients on dialysis in the UK is around 18,400 with up to a
third of these patients affected by SHPT that has not responded to traditional therapies.6

Dr Richard Fluck, Consultant Renal Physician, Derby Hospitals Foundation NHS Trust
commented, “SHPT can be a debilitating condition for people with end stage renal failure,
with existing therapies often unsuccessful in treating this condition effectively. The advent of
cinacalcet has helped to increase SHPT treatment options for patients and as a result,
today’s NICE announcement is likely to be welcomed by all those affected by this condition.”

Cinacalcet works on the parathyroid gland, reducing the secretion of PTH and subsequently
lowering serum calcium and phosphorus levels in dialysis patients with SHPT.7 A published
study has shown that patients taking cinacalcet plus standard therapy are less likely to
experience bone fractures, cardiovascular hospitalisation, or surgery to remove their
parathyroid gland, than those taking placebo plus standard therapy.8

Tim Statham, Chief Executive of the National Kidney Federation, explained, “For many years
renal patients have searched for a solution to help them achieve better control of the mineral
balance in the body. They have needed a treatment that decreases their pain and improves
their quality of life. The treatment of a condition such as SHPT has been overlooked for too
long, until now.”

Treatment of kidney failure and its complications, including SHPT, was made an NHS priority
in 2001 by the National Service Framework (NSF) for renal services. The treatment of
clinically relevant hyperparathyroidism is also recommended in recent guidelines published
by the Royal College of Physicians on anaemia management in chronic kidney disease.9

“Amgen is delighted that the UK’s commitment to improving the treatment of kidney failure
has been further reinforced with today’s NICE announcement on cinacalcet,” explained Dr
Charles Brigden, Medical Director at Amgen.

Secondary Hyperparathyroidism (SHPT)

Secondary hyperparathyroidism (SHPT) is a complex complication of end stage renal disease,
involving abnormalities of parathyroid hormone (PTH), calcium, phosphorus and calcium-phosphorus
product. Factors in the development of SHPT are decreased production of calcitriol (the active form of
vitamin D) by the kidneys leading to hypocalcaemia (low calcium levels). Increased renal phosphorus
retention, leading to hyperphosphataemia, can also occur due to the kidneys’ inability to excrete it
effectively. This in turn leads to excess PTH secretion and eventually increased parathyroid gland
size.

End Stage Renal Disease (ESRD)

End stage renal disease is a complete or near complete failure of the kidneys to function. It usually
occurs as chronic renal failure worsens to the point where kidney function is less than 10% of normal.
At this point, the kidney function is so low that without dialysis or kidney transplantation, complications are multiple and severe, and death will occur from accumulation of fluids and waste products in the body.

About cinacalcet

In clinical trials in secondary HPT patients on dialysis, cinacalcet HCl was well-tolerated and effective
in reducing PTH, Ca, P, Ca x P in a broad range of patients regardless of age, gender, dialysis
method (hemo- or peritoneal dialysis), years on dialysis or disease severity.7

In a clinical trial in patients with hypercalcemia due to parathyroid carcinoma, cinacalcet HCl
significantly lowered calcium levels in the majority of patients.10

Studies have shown that cinacalcet HCl lowers Ca, based on its mechanism of action, so it should not
be initiated if a patient’s Ca levels are below the lower limit of the normal range.10 During dose titration,
Ca levels should be monitored frequently and if levels decrease below the normal range, appropriate
steps should be taken to increase Ca levels. The threshold for seizures may be lowered by reductions
in Ca levels and, infrequently, seizures have been reported. The most commonly reported side effects
are nausea and vomiting.10

About Amgen

Amgen discovers, develops and delivers innovative human therapeutics. A biotechnology pioneer
since 1980, Amgen was one of the first companies to realize the new science’s promise by bringing
safe and effective medicines from lab, to manufacturing plant, to patient. Amgen therapeutics have
changed the practice of medicine, helping millions of people around the world in the fight against
cancer, kidney disease, rheumatoid arthritis, and other serious illnesses. With a broad and deep
pipeline of potential new medicines, Amgen remains committed to advancing science to dramatically
improve people’s lives. To learn more about our pioneering science and our vital medicines, visit
amgen.

References:

1. Kim J et al, EDTA-ERA XLI Congress 2004; Abstract Book 12a, Abstract SO26.
2. Ganesh SK et al, J Am Soc Nephrol 2001 12 2131-2138.
3. Goodman WG et al, New Eng J Med 2000 342 1478-1482.
4. De Boer IH, Gorodetskaya I, Young B et al, J Am Soc Nephrol 2002 13 2762-9.

5. Block GA et al, J Am Soc Nephrol 2003 15 2208-2218.
6. UK Renal Registry, 8th Annual Report 2005 (renalreg).
7. Moe SM, Chertow GM, Coburn JW et al. Kidney International. 2005;67:760-71.
8. Cunningham J, Danse M, Olson K et al. Kidney International, 2005; 68:1793-1800.
9. Anaemia Management in Chronic Kidney Disease. National clinical guideline for management in
adults and children, 2006. p63, paragraph R17.
10. Mimpara® Summary of Product Characteristics.

UroToday- Well recognized potential side effects of androgen deprivation therapy include anemia, decreased libido, the metabolic syndrome, memory loss, weight gain, hot flashes, and osteoporosis. Since periodontal disease results in absorption of alveolar bone, some have suggested that generalized bone mineral loss may exacerbate periodontal disease. The relationship between androgen deprivation therapy and periodontal disease has not been studied.

In the March issue of the Journal of Urology, Famili and colleagues from the University of Pittsburg compared the incidence of periodontal disease in men with prostate cancer treated with or without androgen deprivation therapy.

A total of 81 men with prostate cancer and a mean age of 68.5 years enrolled in the study. Sixty-eight men with prostate cancer underwent periodontal examinations, including 27 men not receiving androgen deprivation (non-ADT) and 41 men on androgen deprivation therapy (ADT). There was no difference between groups with regards to race, history of smoking, previous dental visits, missing teeth, denture use, dental hygiene, or previous periodontal disease. Of these 68 men, 81% of men receiving androgen deprivation therapy were found to have periodontal disease, compared with 3.8% in the non-ADT group (Hazard ratio = 3.33, 95% CI 1.07 to 10.3, p < 0.038). This three-fold increase in periodontal disease was significant even after adjusting for race, history of smoking, or previous periodontal treatment. Interestingly, bone mineral density was not statistically significantly different between the ADT and non-ADT groups.

This study with a small sample size is the first to suggest that men with prostate cancer receiving androgen deprivation therapy exhibit a three-fold higher risk of periodontal disease compared with controls. While the authors suggest that alveolar bone osteoporosis may account for this effect, no differences were found in bone mineral density between groups. These data should be confirmed in a larger cohort of patients to further clarify its etiology and potentially identify measures of prevention for patients embarking on androgen deprivation therapy.

Famili P, Cauley JA, Greenspan SL

J Urol 2007 Mar; 177(3):921-4.
Reviewed by UroToday Contributing Editor Ricardo F. SГЎnchez-Ortiz, MD

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The level of nutrients in soil determines how many different kinds of plants and trees can thrive in an ecosystem, according to new research published by biologists and mathematicians in Nature.

For the first time ever mathematicians have modelled all the different possible relationships between nutrients and biodiversity in lab-based experimental ecosystems. They found that although nutrient availability definitely has an impact on biodiversity, the precise relationship between the two depends on which species are present in the ecosystem. This means that in some cases low levels of nutrients can lead to high levels of biodiversity.

The new study involved biologists from the University of California Santa Cruz running a lab experiment to find out how different levels of nutrients affected how many species evolved in an ecosystem. Mathematicians from Imperial College London and the University of Bath then devised a model to show how far the results could be applied to real world scenarios.

The experiments set up by the biologists in the USA consisted of mini ecosystems full of E. coli bacteria and a parasite that lives on the E. coli. These simple communities of hosts and pathogens represent complex ecosystems in the real world, like forests, in which hosts such as trees live and evolve alongside pathogens such as fungi, bacteria and viruses.

The overall aim of the study was to shed new light on the mystery of why some ecosystems such as tropical rainforests are teeming with thousands of different plant species, whereas others, like the pine forests of northern Europe, support significantly fewer types of plant life. However, investigating this phenomenon in the field can be difficult, time consuming and results hard to interpret.

Instead, the researchers used the series of mini-ecosystems in the lab, which consisted of test tubes containing E. coli bacteria, a sugary Lucozade-like liquid for the Eli to eat, and a parasite that lives on the E. coli.

To mimic different environments, the scientists varied the amount of sugar in each different ‘ecosystem’, and then recorded how many new strains of bacteria and parasite evolved in the sugary broth over the course of 150 generations, which took 17 days.

Their results showed that as the levels of sugar in the ecosystem changed, so did the extent to which new strains evolved. This experiment showed that the highest biodiversity resulted from a low level of nutrients.

Professor Laurence Hurst from the University of Bath’s Department of Biology explains: “The results in the lab showed that varying the level of sugary food in these mini-ecosystems caused the amount of biodiversity in the ecosystems to change. This suggests that the availability of nutrients is one of the factors that affect how many different plant species live in different parts of the world. This has been shown in a lab before, but what we wanted to do was use maths to show how these results, which refer to one kind of bacteria and its parasite, can be applied to other organisms and ecosystems in the real world.”

The team from Bath and Imperial constructed a model to work out whether this inverse relationship would be the same in all ecosystems – whether in the lab or in the real world. They found that although nutrients do affect biodiversity, the precise relationship between the two varies from one ecosystem to the next, depending on what species are present.

Dr Rob Beardmore from Imperial College London’s Department of Mathematics explains: “Although there was a clear link between nutrients and biodiversity in the lab, our mathematical model showed that in some ecosystems you will find that higher levels of nutrients lead to more biodiversity, which is opposite to what our biologist colleagues found in the lab. It turns out that the precise nature of this nutrient-diversity relationship varies from one ecosystem to another, and it depends on the complex interactions between species evolving alongside each other.”

The mathematical model can be used to predict what impact different levels of nutrients will have on biodiversity in any given lab-based ecosystem. The team say their results are very important for scientists who use small scale lab experiments to investigate phenomena in the real world.

The study also provides the first real evidence that a theory known as “geographic mosaic co-evolution hypothesis” holds up in real world ecosystems. Co-author on the paper, Dr Ivana Gudelj from Imperial College, explains: “This complicated-sounding theory basically says that nutrient availability will only have an impact on the diversity of an organism, if the organism is involved in a co-evolutionary arms race with pathogens or competitors, like our Eli was with its parasite. Our biologist colleagues have shown evidence for this in the lab, and our mathematical model suggests that the theory will also hold up in real world ecosystems too.”

###

Source: Danielle Reeves

Imperial College London

Malaria causes more than two million deaths each year, but an expert multinational team battling the global spread of drug-resistant parasites has made a breakthrough in the search for better treatment. Better understanding of the make-up of these parasites and the way they reproduce has enabled an international team, led by John Dalton, a biochemist in McGill’s Institute of Parasitology, to identify a plan of attack for the development of urgently needed new treatments.

Malaria parasites live inside our red blood cells and feed on proteins, breaking them down so that they can use the proceeds (amino acids) as building blocks for their own proteins. When they have reached a sufficient size they divide and burst out of the red cell and enter another, repeating the process until severe disease or death occurs. Dalton and his colleagues found that certain “digestive enzymes” in the parasites enable them to undertake this process. Importantly, the researchers have also now determined the three-dimensional structures of two enzymes and demonstrated how drugs can be designed to disable the enzymes.

“By blocking the action of these critical parasite enzymes, we have shown that the parasites can no longer survive within the human red blood cell,” Dalton explains. The discovery will be published in the Proceedings of the National Academy of Sciences, and is the result of collaboration including Australia’s Queensland Institute of Medical Research, Monash University and the University of Western Sydney, Wroclaw University of Technology in Poland and the University of Virginia in the U.S. The team is putting their findings into action immediately and is already pursuing anti-malarial drug development.

Source: McGill University

The Marburg virus, like its fearsome cousin Ebola, belongs to the Filoviridae family. It carries the name of the German town where it was first detected in 1967, after a mysterious epidemic had hit employees of the Behring laboratory. The workers had been contaminated as they took organ samples from green monkeys imported from Uganda. Up to the end of the 20th Century, rare cases of violent haemorrhagic fever attack linked to Marburg virus were subsequently registered, essentially in East Africa: (in Kenya, Zimbabwe, parts of South Africa). However, in 1998, a more extensive epidemic affected 149 people near Durba, a town in the North-East of the Democratic Republic of Congo (DRC). More than 80% of these people succumbed to the haemorrhagic fever the virus caused. In 2005, a second epidemic that broke out in Angola infected over 252 people, 227 of whom died – a mortality rate of nearly 90%. That was the most severe epidemic of Marburg haemorrhagic fever (MHF) known to date.

Between 2005 and 2006, scientists from IRD working in conjunction with CIRMF and CDC conducted a research campaign with the aim of detecting Ebola virus among species of fruit bat (mammals of the order Chiroptera). In the context of this study, five trapping sites were set up in the tropical rainforest of Gabon and the North-West of the Democratic Republic of Congo. The 1138 specimens of fruit bat collected belong to 10 different species. At the same time, Angola, about 800 km from the study area, experienced a severe outbreak of MHF. However, the natural reservoir of this virus was still unknown. In addition to the search for Ebola in each of the chiropteran specimens caught, the researchers looked for the presence of its cousin in their tissues. A series of analyses were performed on the bats captured: detection of viral RNA in the liver and spleen by various methods of nucleotide amplification; a search for Marburg virus-specific antibodies in the blood; phylogenetic characterization of amplified genomic fragments.

The analyses detected antibodies directed against Marburg virus in the serum of just one of the 10 species caught, the Egyptian rousette, Rousettus aegyptiacus, (in 29 out of 242 individuals tested). This is a migratory species whose distribution range includes all parts of the African continent situated South of the Tropic of Cancer. The search for viral genome fragments on 283 specimens of R. aegyptiacus showed the liver and spleen of four of them to contain RNA sequences belonging to 3 different Marburg virus genes. Blood serum of three out of the four specimens also contained Marburg virus-specific antibodies. The simultaneous presence of specific antibodies and viral RNA fragments strongly suggested this bat species’ role as a non-symptom developing carrier of the virus, indicating R. aegyptiacus to be the natural reservoir.

Previous research on Ebola virus showed that human infection comes about through the intermediary of infected great ape carcasses. The viral transmission to primates occurs in the dry season, a period when food resources become increasingly scarce.

The great apes then come into competition with bat species for fruit supplies when foraging and can be infected notably by blood or by placental fluid that escapes when bats give birth. The mode of contamination by Marburg virus appears to be different, however. It does not appear to need any intermediary to be pathogenic for humans, as foreseen from data of the latest two epidemic outbreaks. In one outbreak, which raged in the north-east of DRC in 2000, most people infected worked in a goldmine, which turned out to be the refuge for a large colony of Egyptian rousettes. During the second epidemic, in Angola, the first victims were children who had gathered fruit from trees where a large population of this species of fruit bat roosted. Other evidence was the fact that the capture sites chosen for this study were all located near caves harbouring sizeable groups of these bats. Moreover, the discovery of such bats that were carriers of Marburg virus in Gabon, a country where no clinical case has yet been recorded, gives an incentive for setting up surveillance and prevention measures in regions where no MHF virus epidemic has ever occurred.

The findings should be useful in the future for defining more accurately the geographical areas potentially affected by Marburg virus. They could also help in extended studies, particularly in West Africa, a significant region for migration of Rousettus aegyptiacus. This identification of the virus’s natural reservoir should also favour the development of public health measures and prevention strategies involving local people which could minimize the infection potential of possible MHF epidemics to come.

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UroToday- This article published in the September issue of Urology details the feasibility of bladder preservation with muscle-invasive cancer using transurethral resection alone. The authors evaluated 327 patients with muscle-invasive bladder cancer who were treated in at M.D. Anderson from 1997 to 2002. Repeat bladder tumor resection was repeated in all patients. If the patient had no residual tumor on biopsy, normal examination under anesthesia, and normal upper urinary tracts bladder preservation was offered. Patients who opted for bladder preservation by transurethral resection alone did not receive intravesical therapy and were followed up by routine cystoscopy for a median of 2.45 years.

Of 327 patients, 35 (11%) were eligible for bladder preservation, 27 elected to pursue this approach and 8 opted for immediate cystectomy. Of the 8 that underwent immediate cystectomy 4 had no residual tumor and one died from metastatic disease. Of the 27 patients who did have bladder preservation, 15 experienced subsequent tumor recurrence, 8 of whom underwent radical cystectomy. Of the 8 that had a delayed cystectomy 4 had node positive disease and 5 had extravesical disease. Only one of the delayed cystectomy patients had organ-confined disease without nodal extension and that person underwent neoadjuvant chemotherapy. The overall and disease-specific survival rate was 81% and 93%, respectively but 2 are alive with metastatic disease.

Bladder preservation using transurethral resection is feasible in selected patients, only 11% of the eligible population. Unfortunately, despite close surveillance 30% needed a cystectomy and of these 8 patients 50% had node positive disease and 62% had extravesical disease. This highlights that our current surveillance programs are inadequate to identify recurrent bladder cancer at a curable stage.

Leibovici D, Kassouf W, Pisters LL, Pettaway CA, Wu X, Dinney CP, Grossman HP

Urology. 70(3): 473- 476, September 2007
doi:10.1016/j.urology.2007.05.007

Reported by UroToday Contributing Editor David P. Wood, M.D

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