The air in Beijing during the 2008 Olympics was cleaner than the previous year’s, due to aggressive efforts by the Chinese government to curtail traffic, increase emissions standards and halt construction in preparation for the games, according to a Cornell study.

Led by Max Zhang, assistant professor of mechanical and aerospace engineering, the study indicates that such measures as regulating traffic density and encouraging public transportation can have a significant impact on local air quality.

“We hope our study can help or advise local regulators and policymakers to adopt long-term sustainable emission controls to improve air quality,” Zhang said. “That’s our mission.”

Published online recently in the journal Atmospheric Environment, the study was based on air quality readings before, during and after the Olympics. Leading up to the Olympics, the Chinese government barred more than 300,000 heavy-emission vehicles — mostly trucks — from the roads. The city also implemented rules in which only some people were allowed to drive on certain days based on their license plate numbers. As a result, close to 2 million vehicles were pulled from the roads. Other mandates involved halting construction and decreasing the use of coal in favor of natural gas for electricity.

In 2007 and 2008, the researchers collected air quality data from equipment installed at two elevations on a building in the heart of Beijing.

They also tracked emissions from vehicles in different areas of the city by following randomly selected cars and trucks in a minivan equipped with sensitive instruments for detecting carbon particles, including carbon monoxide, carbon dioxide and black carbon, or soot.

Among the researchers’ conclusions: Black carbon pollution is significantly greater at ground level than at higher elevations, and diesel trucks are a major source of black carbon emission during the summer in Beijing. These particles are not only harmful to the lungs, but are also known to be a global warming compound, Zhang said.

The researchers found that car emissions of black carbon were down 33 percent in 2008 compared with their 2007 readings. Carbon dioxide decreased 47 percent, and ultrafine carbon-based particles — those that measure less than 100 nanometers — decreased 78 percent.

The sharp drops were most likely due to a new emission standard implemented in Beijing in 2008, in which all new registered vehicles as well as gasoline and diesel fuel engines were required to achieve emissions standards equivalent to European Union regulations. A similar standard was mandated starting in June 2008 for 20,000 buses and 66,000 taxies. The improved fuel quality probably enhanced the performance of engines and catalytic converters, the researchers reported.

“We are showing what the city can do if they are determined to improve air quality,” Zhang said.

The study, whose first author was graduate student Xing Wang, was funded by the U.S. Environmental Protection Agency and Cornell’s Jeffrey Sean Lehman Fund for Scholarly Exchange with China.

By Anne Ju

Source:
Blaine Friedlander

Cornell University

Like cats, human cells have a finite number of lives-once they divide a certain number of times (thankfully, more than nine) they change shape, slow their pace, and eventually stop dividing, a phenomenon called “cellular senescence”.

Biologists know that a cellular clock composed of structures at the chromosome end known as telomeres records how many “lives” a cell has expended. Up to now, investigators have not yet defined how the clock’s ticking signals the approach of cellular oblivion.

In a study published in the Oct. 3, 2010, issue of Nature Structural and Molecular Biology, a team led by Jan Karlseder, Ph.D., at the Salk Institute for Biological Studies reports that as cells count down to senescence and telomeres wear down, their DNA undergoes massive changes in the way it is packaged. These changes likely trigger what we call “aging”.

“Prior to this study we knew that telomeres get shorter and shorter as a cell divides and that when they reach a critical length, cells stop dividing or die,” said Karlseder, an associate professor in the Molecular and Cell Biology Laboratory. “Something must translate the local signal at chromosome ends into a huge signal felt throughout the nucleus. But there was a big gap in between.”

Karlseder and postdoctoral fellow Roddy O’Sullivan, Ph.D., began to close the gap by comparing levels of proteins called histones in young cells-cells that had divided 30 times-with “late middle-aged” cells, which had divided 75 times and were on the downward slide to senescence, which occurs at 85 divisions. Histone proteins bind linear DNA strands and compress them into nuclear complexes, collectively referred to as chromatin.

Karlseder and O’Sullivan found that aging cells simply made less histone protein than do young cells. “We were surprised to find that histone levels decreased as cells aged,” said O’Sullivan, the study’s first author. “These proteins are required throughout the genome, and therefore any event that disrupts this production line affects the stability of the entire genome.”

The team then undertook exhaustive “time-lapse” comparisons of histones in young versus aging cells and confirmed that marked differences in the abundance and variety of histones were evident at every step as cells moved through cell division.

O’Sullivan calls the “default” histone pattern displayed by young cells “happy, healthy chromatin.” By contrast, he says, aging cells appear to undergo stress as they duplicate their chromosomes in preparation for cell division and have difficulty restoring a “healthy” chromatin pattern once division is complete.

Comparisons of histone patterns in cells taken from human subjects-a 9- versus a 92-year-old-dramatically mirrored histone trends seen in cell lines. “These key experiments suggest that what we observe in cultured cells in a laboratory setting actually occurs and is relevant to aging in a population,” says Karlseder.

The initiation of diseases associated with aging, such as cancer, is largely attributed to DNA, or genetic, damage. But this study suggests that aging itself is infinitely complex: that progressive telomere shortening hastens chromosomal aging by changing the way genes entwine with histones, so-called “epigenetic” changes. How DNA interacts with histones has enormous impact on whether genes are expressed-hence the current intense interest in the relationship of the epigenomic landscape to disease states.

Rescue experiments in which the team cosmetically enhanced aging cells confirmed that signals emitted by eroding telomeres drove epigenetic changes. When aging cells were engineered to express telomerase, the enzyme that restores and extends stubby telomeres, those rejuvenated cells showed histone levels reminiscent of “happy, healthy chromatin,” and a partial return to a youthful chromatin profile.

Lest you sink your savings into schemes to elongate your telomeres, beware. “The flip side of elongating telomeres is that you enable cells to grow for much longer periods and can generate what are called “immortal” cells,” says Karlseder. “That takes you one step closer to cancer cell development.”

Up to now, the Karlseder lab has mostly focused on interactions between telomeres and DNA repair mechanisms. This paper now pushes them into the field of epigenetics. “We will continue to examine epigenetic changes in cells at different ages,” says Karlseder. “We now want to determine if histone changes follow a linear process or whether they kick in as we age.”

Also contributing to this work were Stuart Schreiber, Ph.D., of the Broad Institute of Harvard and MIT and Howard Hughes Medical Institute and his postdoctoral fellow Stefan Kubicek, Ph.D.

The study was funded by the National Institutes of Health, the George E. Hewitt Foundation for Medical Research, and the Ernst Schering Research Foundation and the European Union.

Source:
Salk Institute

UroToday – We used our relatively extensive experience to evaluate retrospectively the safety and efficacy of salvage brachytherapy for the treatment of locally recurrent prostate cancer after external beam radiotherapy.

Prior studies demonstrated significant morbidity to this therapy, however that does not seem to be true in our hands. We found this therapy, at least in the short to intermediate term, to be an effective treatment modality with low morbidity (no fistula formation).

Likely our success is due to careful planning and technique which includes the use of magnetic resonance spectroscopy and avoidance of high radiation dosage to the rectum or urethra.

David Aaronson, MD as part of Beyond the Abstract on UroToday

UroToday – the only urology website with original content global urology key opinion leaders actively engaged in clinical practice.

To access the latest urology news releases from UroToday, go to:
www.urotoday

Copyright © 2009 – UroToday

UroToday- A history of smoking is associated with an increased risk of metastatic disease in patients treated with radiotherapy (XRT) for prostate cancer (CaP), according to a report in the online version of the BJU International. The work is published by Dr. Pantarotto and colleagues in Ottawa, Canada.

In this retrospective review, 434 patients were treated with 66Gy of definitive radiotherapy between 1990 and 1999. To be included, patients had a PSA level 6 months smoking history but not smokers at time of consultation) or current smokers. Biochemical failure was defined by ASTRO criteria. Data regarding time to biochemical failure, time to local failure, time to distant failure, overall survival and disease-specific survival were generated.

A smoking history was obtained in 416 of 434 patients (96%) and the lifetime prevalence of smoking was 71%. Current smokers constituted 17% and non-smokers 29% of the cohort. Median follow-up was 70 months and current smokers presented at a younger median age of 66.4 years, compared with 69.9 years for previous smokers and 70 years for non-smokers. Clinical T stage, Gleason score and initial PSA were not significantly different between the smoking categories.

Biochemical, local and distant failure occurred in 44.6%, 23.2%, and 15.5% of patients, respectively. While biochemical and local failure rates were similar among smoking groups, a higher proportion of current smokers had distant failure events. Disease-specific survival was not significantly different among the three smoking groups, whereas overall survival was worse for current smokers than non-smokers (46% vs. 26%). The cohort death rate was 34%, with 39% of those deaths due to CaP. In univariate analysis, both previous and current smoking was associated with higher distant failure rates. In multivariate analysis, previous and current smokers had a higher risk of distant failure, 2.90 and 5.24, respectively. Overall and CaP-specific survival were not significantly different among the three smoking groups.

Several mechanisms have been proposed regarding the impact of smoking on CaP patient outcomes to XRT. Smoking-induced hypoxia secondary to high serum carboxyhemoglobin levels that interfere with hemoglobin-oxygen dissociation is thought to significantly contribute. Smoking also likely affects cellular mechanisms that result in tumor progression.

Jason Pantarotto, Shawn Malone, Simone Dahrouge, Victor Gallant and Libni Eapen

BJU Int 2006; 99(3): 564-569
Reviewed by UroToday Contributing Editor Christopher P. Evans, MD

UroToday – the only urology website with original content global urology key opinion leaders actively engaged in clinical practice.

To access the latest urology news releases from UroToday, go to:
www.urotoday

Copyright © 2006 – UroToday

Scientists at Albert Einstein College of Medicine of Yeshiva University have received a five-year, $10.8 million grant to develop stem cell-based therapies that could be used to mitigate radiation induced gastrointestinal syndrome part of acute radiation syndrome (ARS) for military personnel, first responders and the general public. The Einstein research, funded by the federal Centers for Medical Countermeasures Against Radiation, is part of a program coordinated by the National Institute of Allergy and Infectious Diseases.

“This type of research fills a special need,” said lead investigator Chandan Guha, M.B.B.S., Ph.D. , professor and vice chair of radiation oncology at Einstein and Montefiore Medical Center. “Currently, post-event strategies for responding to ARS must be carried out within the first several hours of an event, and those strategies have demonstrated only marginal protection.” At present, there are no Food and Drug Administration (FDA)-approved treatments that can effectively treat ARS. For first responders and others, this lack of protection against the effects of radiation could be fatal.

Radiation protection is a natural research avenue for Dr. Guha and his radiation oncology colleagues. Killing cancer cells with radiation therapy or chemotherapy must be done in ways that minimize toxicity to the rest of the body.

“When radiation is used in combination with chemotherapy for head and neck cancer or cervical cancer, it is very successful,” said Dr. Guha. “But the same cannot be done for cancers in the abdomen. High doses of radiation cannot be administered effectively to that area because radiation is very toxic to the intestines and the liver. This is the same sort of toxicity that occurs in radiation-induced gastrointestinal syndrome.”

Radiation to the abdomen can cause intestinal cells to begin dying within hours. The result is a loss of the intestine’s protective mucosal lining, microbial infection, septic shock, and an inflammatory response that affects the entire body. Death is dose dependent and can occur within days following exposure.

In earlier research, Dr. Guha has shown that animals receiving lethal doses of radiation to their abdomen can be rescued by intravenous transplantation of bone marrow-derived stromal cells. Using their bone marrow-derived stem cell transplant technique, Einstein scientists have saved animals exposed to a radiation dose of 18-20 Gy equal to more than 2.5 times their lethal dose. The transplant was successful in saving these animals from fatal radiation injury even when administered 24 hours after radiation exposure. This cell therapy is believed to create conditions that allow irradiated intestinal stem cells to recover.

The new grant will allow Einstein researchers to develop their bone marrow transplant technique with the goal of saving people suffering from radiation-induced gastrointestinal failure. Further research will be performed to identify chemical agents that accelerate repair and regeneration of stem cells exposed to irradiation.

A small portion of the grant will fund the work of Dr. William Fleming, M.D., Ph.D., of the Oregon Health & Science University, Portland, OR. He will look at treating radiation-induced bone marrow syndrome with endothelial progenitor cells. The grant also supports core facilities at Einstein for histopathology (Rani Sellers, Ph.D.) and metabolomics (Erwin Kurland, M.D. Ph.D.) and Stony Brook University Medical Center, Stony Brook, NY for proteomics (Emily Chen, Ph.D.) to support the work of Drs. Guha and Fleming.

Source: Albert Einstein College of Medicine of Yeshiva University

Australian researchers have published the results of a study, for the first time showing a positive effect of growth hormone on athletic performance.

It showed a .4 second improvement in a 10-second sprint, enough to turn a last-place Olympic athlete in a sprint event – running or swimming – into a Gold medal winner.

The study justifies growth hormone being a banned substance, even though evidence of its performance enhancing effect has been very poor until now.

Growth hormone, produced naturally in the body, is important for growth and metabolism. Injectable growth hormone is available for people who have growth hormone deficiency. Many athletes use the drug because they believe that it bulks up their muscles and improves their physical performance (growth hormone “doping”). Until this study, no scientific research had been undertaken to show that growth hormone improves physical performance.

Researchers at Sydney’s Garvan Institute of Medical Research demonstrated that growth hormone increases an athlete’s ability to sprint on a bicycle, but has no effects on fitness, weight lifting or jumping. The effect on sprint capacity nearly doubled in men who received testosterone injections in addition to growth hormone supplementation.

The study looked at 103 healthy recreational athletes, aged 18 to 40 years, who had engaged in regular athletic training for at least a year. It was double-blind and placebo-controlled, meaning that neither the investigators nor the participants knew who was receiving the drug or dummy injections (salt water).

Professor Ken Ho, head of pituitary research at Garvan, as well as Chairman of the Department of Endocrinology at St. Vincent’s Hospital, undertook the project with Drs Udo Meinhardt and Anne Nelson, as members of a larger team. Their findings are published today in the prestigious international journal, Annals of Internal Medicine.

“Those athletes given growth hormone improved their sprint capacity by 4-5%,” said Professor Ho.

“Growth hormone recipients did not increase their muscle mass. They did, however, retain body fluid and experienced swelling and joint pain, unlike those who received salt water injections.”

“We used lower doses of growth hormone than athletes are reported to use, and for a shorter time. We can speculate, therefore, that the drug’s effects on performance might be greater than shown in this study, and its side effects might be more serious.”

“In conclusion, growth hormone increases athletic sprinting when given alone or in combination with testosterone. This is the first demonstration of improvement in a selective aspect of physical performance with growth hormone. We believe that this effect may bring a competitive advantage to athletes engaging in sprint events.”

This work was funded by the World Anti-Doping Agency.

Source:
Research Australia

Not even the most avid fans could notice, but those spectacular aerial images of a brightly-lit Cowboys Stadium during Sunday’s Super Bowl XLV symbolize one of the hottest new pieces of scientific intelligence about air pollution:

Researchers have discovered – in a classic case of scientific serendipity – that the bright light from sports stadiums and urban street lights may boost daytime levels of ozone, a key air pollutant in many heavily populated areas. That’s among the topics included in a broader article about the chemistry of air pollution in Chemical & Engineering News (C&EN), ACS’ weekly newsmagazine.

In the article, C&EN Associate Editor Jyllian Kemsley describes a so-called “field campaign” that took place in southern California and Mexico last year. It was a far-ranging effort by land, sea, and air to gain a deeper scientific understanding of all the factors involved in air quality and climate change. One of experiments involved use of detectors to measure the intensity of sunlight from an airplane.

As the plane flew over a brightly lit sports stadium, one of the crew suggested, perhaps only half seriously, turning the device on, even though it was the dead of night. Much to the scientists’ surprise, they found there was enough light to drive certain chemical reactions in the atmosphere that would boost daytime levels of ozone, one of the most prevalent and difficult-to-control air pollutants in urban areas. One of the scientists in the experiment notes in the article that cities and states, struggling to meet ever-stricter government air pollution limits, may want to consider the unexpected effects of night-time lighting of streets, sports stadiums, and other sources of bright light.

ARTICLE: “Monitoring the Skies”

Source:
Michael Bernstein
American Chemical Society

For the millions of people who suffer from urinary tract infections each year and the doctors who treat them, a promising new biosensor technology has been developed that may replace antiquated testing methods and save precious health care dollars.

In a recent clinical study conducted by the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System, researchers used a biosensor developed by corporate partner GeneFluidics to identify correctly the infection-causing gram negative bacteria species in 98 percent of the tested clinical urinary tract infection urine samples. These results represent the first ever species-specific detection of bacteria in human clinical fluid samples using a microfabricated electrochemical sensor array.

Of equal significance, the new test provided results in 45 minutes, compared to two days with conventional methods.

The research, reported in the February 2006 issue of the peer-reviewed Journal of Clinical Microbiology, investigated a new technology to solve an old problem: the diagnosis of urinary tract infections — the second most common bacterial infection — in a clinically relevant timeframe.

In current laboratory practice, contaminating pathogens in urine specimens are grown in culture dishes until they can be visually identified. The major drawback of this century-old technique is the two-day time lag between specimen collection and bacteria identification. As a result, physicians must decide whether to prescribe antibiotic therapy and, if so, which type of bacteria to treat — all without knowing the cause of the infection, if any. In contrast, the new biosensor technology would allow physicians to prescribe targeted treatment without the wait.

“Our research also showed that GeneFluidics’ biosensor avoided problems inherent in alternative molecular approaches, such as PCR, that require the repeated copying of bacterial DNA or RNA prior to testing. We found that these amplification methods do not provide reproducible results,” said lead author Dr. Joseph C. Liao, clinical instructor of urology at the David Geffen School of Medicine at UCLA.

The clinical study was performed at the VA Greater Los Angeles Healthcare System in the laboratory of Dr. David Haake, VA staff physician and professor of medicine at UCLA. Researchers studied samples received by the UCLA Clinical Microbiology Laboratory.

Individual sensors on GeneFluidics’ 16-sensor chips were coated with UCLA-designed species-specific genetic probes. Clinical urine samples were directly applied to the chips and the electrochemical signal subsequently measured by GeneFluidics’ multi-channel reader instrument. The urinary tract infection pathogens were identified by examining which signals on the sensor chip were elevated. The entire experiment from sample collection to result read-out took only 45 minutes.

The potential for rapid bacterial detection was discovered in the laboratory of Dr. Edward McCabe, chair of pediatrics at the Mattel Children’s Hospital at UCLA and an adviser to GeneFluidics. McCabe’s group demonstrated that probes could bind to species-specific bacterial sequences within minutes, rather than hours. These exciting results were translated to the biosensor protocol, leading to the development of the biosensor for rapid identification of bacteria in urine from patients with urinary tract infections.

“Results were impressive for this initial 78-sample clinical study,” said Dr. Bernard Churchill, chief of pediatric urology at the Clark-Morrison Children’s Urological Center at UCLA and principal investigator. “By coupling UCLA’s robust probes with GeneFluidics’ ultra sensitive biosensor system, we were able to identify urinary tract infection pathogens in a time frame that would enable physicians to make dramatically superior clinical decisions.”

Ongoing work at UCLA and the VA Medical Center is focused on developing even better detection methods to bring the urinary tract infection biosensor chip from “bench to bedside.” At GeneFluidics, engineers are integrating the biosensors into microfluidic cartridges and building a new instrument for faster and completely automated experimentation. The team anticipates the rapid test could become available in the next two to three years.

“There is considerable interest in decreasing overall health care costs by providing smarter medicine,” added Dr. Vincent Gau, chief executive officer of GeneFluidics. “When laboratory-quality testing can be rapidly performed by anyone, anywhere, and the results made available in ‘real-time,’ we will see tremendous improvement in patient care. This joint project with UCLA may spearhead that shift.”

Urinary tract infection is the most common urological disease in the United States and the most common bacterial infection of any organ system. Urinary tract infection is a major cause of patient death and health care expenditure for all age groups, accounting for more than 7 million office visits and more than 1 million hospital admissions per year. In the hospital, catheter associated urinary tract infection accounts for 40 percent of all in-hospital acquired infections — more than 1 million cases each year. The total cost of urinary tract infections to the United States health care system in 2000 was approximately 3.5 billion dollars.

The collaboration between UCLA, VA and GeneFluidics began in 2001, thanks to initial funding from Frank W. Clark Jr., and the Wendy and Ken Ruby Fund for Excellence in Pediatric Urology Research.

Subsequently, the work has been supported by a $5.6 million Bioengineering Research Partnership grant from the National Institute of Biomedical Imaging and Bioengineering.

###

GeneFluidics was founded in 2000 by Vincent Gau, who received his Ph.D. in biomedical engineering at UCLA. GeneFluidics’ goal is to develop a fast, accurate and simple testing system for improving worldwide health. By integrating novel bionano and microfluidic technologies, the company’s revolutionary platform will enable complex tests that are currently performed by skilled technicians in a laboratory to be performed by anyone, anywhere.

For more than 50 years, the UCLA Department of Urology has continued to break new ground and set the standards of care for patients suffering from urological conditions. In collaboration with UCLA’s eminent research scientists, their internationally acclaimed physicians have pioneered treatments for many conditions, including cancers of the prostate, bladder and kidney, kidney stones, pelvic floor disorders, genitourinary tract conditions, incontinence and sexual dysfunction in men and women.

(Note to Editors: B-roll footage and digital images of biosensor test are available.)

Contact: Amy Waddell
awaddellmednet.ucla.edu
University of California – Los Angeles

A class of drugs thought to kill cancer cells may in fact block “cross talk” between the cancer cell and normal immune cells, resulting in reduced cancer growth and spread – a discovery that could significantly alter the way cancer drugs are evaluated in the future.

Researchers at the University of Colorado Cancer Center demonstrated the discovery in bladder cancer, the fifth most common cancer in the United States. Bladder cancer will kill about 14,000 Americans this year, most of whom will die as a result of the disease’s spread to other organs in a process called metastasis.

The scientists showed that endothelin-A receptor antagonist drugs are only effective at blocking the start of cancer spread to other organs, not treating large, established primary-or distant-site tumors. The study was published online in the Journal of Clinical Investigation.

“We discovered that these drugs block the ‘tumor host interactions’ found at sites of metastasis, which is what reduces tumor growth at these sites,” said lead author Dan Theodorescu, MD, PhD, director of the University of Colorado Cancer Center and professor of surgery and pharmacology at the University of Colorado School of Medicine. “However, unless the drugs are used early, they have minimal or no effect.”

Endothelin-A receptor antagonist drugs block the action of a protein called endothelin 1 [ET-1], thought to be involved in stimulating cancer cell growth and spread. Theodorescu’s lab discovered that ET-1 attracts immune cells called macrophages to cancer cells lodged in the lungs. The macrophages start making factors that stimulate the cancer cells in the lungs to grow – called metastatic colonization – which significantly decreases the patient’s chance of survival.

In the past decade, two endothelin-A receptor antagonist drugs – Abbott’s atrasentan and AstraZeneca’s zibotentan – have had difficulties in large phase 3 clinical trials. Both drugs were tested in a large number of patients with advanced cancer, and neither drug attained its desired effects. Most likely, Theodorescu said, the drugs were given after the window of opportunity for them to work had closed.

“Had we known this before the trials, we wouldn’t have used them to try to reduce large, established tumors,” he said. “We would have used them to try to suppress the appearance of metastasis. This new information has important implications for how we test drugs for effectiveness before human use and then on how we select patients in clinical trials with these agents, especially since many types of cancer secrete ET-1.”

Source:
Caitlin Jenney
University of Colorado Denver

Elsevier and the Royal Tropical Institute (KIT) in Amsterdam announced on 26th of August the signing of a Memorandum of Understanding (MoU) providing 150 researchers working in least-developed and low-income countries (for example Benin, Mozambique, Ethiopia, Togo etc.) with access to ScienceDirect and Scopus, Elsevier’s online scientific research platform and flagship abstract and citation database. Active in fields such as tropical medicine and sustainable development, the scientists are able to apply the information available in ScienceDirect and Scopus to the treatment and prevention of diseases such as HIV/AIDS, malaria and tuberculosis; promoting rural development with improved water, sanitation and food security in addition to other areas relevant to the UN Millennium Development Goals.

Elsevier and KIT’s department Information & Library Service (KIT ILS) in Amsterdam are collaborating on this unique public-private partnership to drive capacity building in information technology and management in the developing world. The new agreement will expand access for five years while sharing best practice in research and training.

As an integral part of this initiative, KIT ILS facilitates a closed Virtual Knowledge Community on information management to share best research practices and identify issues of common interest. First piloted in 2007, this joint Elsevier – KIT initiative provides the Virtual Knowledge Community members in African, Caribbean, Asian and Pacific countries with access to ScienceDirect’s 10 million full-text articles and Scopus’ abstract and citation database containing 18,000 peer-reviewed journals from 5,000 publishers.

“Elsevier and KIT have a long and productive relationship. The continuation of this initiative provides our partners in the South with access to a wealth of information that is directly relevant to their research. The association of the program with the Elsevier Foundation and Research4Life provides both recognition and sustainability. It is a privilege for KIT ILS to act as an intermediary in a co-operative effort that so closely matches our departmental and institutional goals,” said Hans van Hartevelt, Director of KIT Information & Library Services. Jan Donner, CEO of KIT agrees: “This is a unique project which definitely matches our institutional goals. We are very proud that we can realize this together with Elsevier as an innovative co-partner.”

“We are very happy to support the critical work that the Royal Tropical Institute is doing to drive access, usage and authorship in key developing world institutes, bringing key researchers closer to their peers and individual research communities around the world,” said David Ruth, Executive Director of the Elsevier Foundation and Senior Vice President Global Communications, Elsevier. “This carefully targeted initiative is part of our overall effort with Research4Life and the Elsevier Foundation, to provide clinicians, researchers and policymakers in the developing world with access to the information they need to address critical health and sustainability challenges.”

“Good news, extension of access to ScienceDirect and Scopus for five more years. I have been using ScienceDirect to obtain articles for our scientists and this is having a very positive impact on our research. For instance, our output of publications has continued to increase, thanks to access to many journal titles in ScienceDirect.” Thomas Adigun, Head Librarian, Africa Rice Center, Cotonou, Benin.

“ScienceDirect is our sole full-text, up-to-date scientific database to which we have access. Our researchers have greatly benefited from it and it has become an essential source of information for us.” Rose May Ng Kee Kwong, Librarian, MSIRI, Mauritius.

Source:
Ylann Schemm
Elsevier