Monday, December 28, 2009

Annual General Meeting 2009

The 2009 Annual General Meeting will be held on the 29th December 2009 (Tuesday) at 4pm at 87 Park City Commerce Square, 97000 Bintulu (Law office of David Allan Sagah Teng)

Wednesday, December 23, 2009

Season's Greetings

Merry Christmas & Happy New Year!

Friday, November 6, 2009

Natural Science Lecture: Oil Palm & Conservation

The Natural Science Society Presents

"Oil Palm & Conservation : Shall We Do Both?"

by : Mr Rob Stuebing
Technical Advisor (Conservation),
PT. Rea Kaltim Plantations, Samarinda, Kalimantan Timur, Indonesia.

Date: 7th November 2009 (Saturday) 2-4pm

Venue: New World Suite Bintulu Level 5

Free Admission


PRESENTATION OUTLINE:

The presentation deals with the approach to conservation work as set up by PT. REA Kaltim Plantations, a medium-sized oil palm company located in the Mahakam Basin of East Kalimantan, Indonesia. Since 1994, about 26,000 hectares of oil palm have been planted, while 19.5% of the land has been set aside for the conservation of biodiversity.

Mr. Rob Stuebing has worked as the Technical Advisor since setting up the REA Kaltim Conservation Department (REA KON) in late 2007.

The official policy of the PT REA Kaltim as presented by this Department is to:
• Conserve the biodiversity features of the original landscape;
• Minimise or eliminate adverse ecological impacts of human activities;
• Provide long-term benefits for all.

REA KON maintains long-term scientific partnerships or MOUs with the Indonesian Institute of Science, as well as several local universities (Universitas Indonesia in Jakarta, and Universitas Mulawarman in Samarinda), local NGOs such as WWF-Indonesia, and international organizations such as the Singapore Herbarium, Field Museum of Natural History and the IUCN Crocodile Specialist Group. PT. REA Kaltim Plantations is a member of RSPO, and has cooperative links with the Rainforest Alliance’s Sustainable Agriculture Network (SAN).

SPEAKER’S PROFILE:

Rob Stuebing arrived in Malaysia as a Peace Corps volunteer in 1973, and in early 1974 began teaching vertebrate biology, ecology and systematics at Universiti Kebangsaan Malaysia (Kuala Lumpur), and subsequently in UPM-Serdang and UKM-Sabah, for about 20 years. After a brief stint as Honorary Curator of Zoology at the Sabah Museum 1992- 1993, he joined the ITTO (International Tropical Timber Organization) Unit of the Forest Department Sarawak in biodiversity surveys and management for Totally Protected Areas and logging concessions. Subsequently, he worked as a consultant for WWF - Indonesia, for DANCED/Sabah Wildlife Department on crocodile management, and back to Kalimantan for Timber Certification with the Rainforest Alliance/SmartWood until 2003. He worked with the Sarawak’s Planted Forests Project as Conservation Manager from 2004-2007. Later in 2007, he was appointed Technical Advisor to the Conservation Department of PT. REA Kaltim Plantations, in Hulu Belayan, East Kalimantan. An aspiring herpetologist, he has published a number of scientific papers on small mammals, frogs, snakes, and crocodiles, as well as two field guides (with Robert F. Inger) on the frogs, and the snakes of Borneo. He also has several former students lurking in the audience.

KEY QUALIFICATIONS

• Six years in developing effective, integrated conservation programmes in the industrial plantations (acacia and oil palm) in Malaysian Borneo and Kalimantan, Indonesia.
• Thirty-five years experience in biodiversity assessment and management of Protected Areas, timber concessions and plantations (Malaysia and Indonesia)
• Member of IUCN/SSC Amphibian Specialist Group, Crocodile Specialist Group, Sustainable Use Specialist Group) and founder member / former Chair (20072008) IUCN/CSG Tomistoma Task Force
• Supervision of faunal inventories, and writing of conservation management plans as a consultant biodiversity specialist for governmental, and NGO/Civil Society, and private companies
• 19 years teaching experience in Malaysian universities.

Thursday, October 22, 2009

Monday, August 10, 2009

Bintulu Rainforest In Art & Photography Exhibition

The Bintulu Rainforest In Art & Photography Exhibition wrapped up on Sunday evening after a very successful nine day run at the Park City Mall in Bintulu.

We had great reception and feedback from the community from Bintulu as well as from Sibu, Miri and other countries.

Thank you to all who supported us to make this event a great success.


Pictures At The Exhibition




Pictures At The Exhibition





Pictures At The Exhibition

Wednesday, August 5, 2009

Sarawak Tourism Minister Visiting The Bintulu Rainforest In Art & Photography Exhibition




5th August 2009 @11am at the Park City Mall Bintulu.




Datuk Michael Manyin, Sarawak's Tourism Minister visited the exhibition this morning accompanied by Mr Keith Pointer, Chief Operating Officer of the New World Suite Hotel and Park City Mall.




Bottom Picture: The Toursim Minister meeting William Taylor, artist whose work in on display at the exhibition.


Top Picture: The minister discussing photography with Joanes Unggang, Head of Grand Perfect Conservation Department.

Tuesday, August 4, 2009

Pictures At The Exhibition











Bintulu Rainforest In Art & Photography Exhibition




At the Bintulu Rainforest Art & Photography Exhibition at Park City Mall
Top picture: Young visitors with Artist William Taylor
Bottom picture: View of the Exhibition


Wednesday, July 29, 2009

Bintulu Rainforest In Art & Photography Exhibition



With the artists this morning at the press release for the exhibition.

Wednesday, July 22, 2009

Bintulu Rainforest In Art & Photography Exhibition

Date: 1st-9th August 2009

Time : 10am to 9pm daily

Venue : Park City Mall

Featuring Artists/Photographers: Chien Lee Wldlife Photographer
Lucas Kueh Artist Acrylic on Canvas
William Taylor Pencil Drawings


Free Admission

Organiser: Natural Science Society Bintulu Sarawak
Sarawak Planted Forest Sdn Bhd

Sponsors: Park City Mall
New World Suite
Oiltown Signcraft

Enquiries to: sarawaknaturalscience@gmail.com

Monday, July 6, 2009

Natural Science Lecture: Viruses: Old And Emerging Threats To Humanity


Viruses have coexisted with humankind since the dawn of our species. They are capable of causing a wide range of illness from colds and runny noses to deadly Ebola hemorrhagic fever. What are they and how do they transmit themselves and make us sick? Does modern medicine offer any protection from these invisible agents? How dangerous is AH1N1 “swine flu”? The answers to these questions and more await."

Speaker Profile:

William Stuebing is a microbiologist who graduated from Miami University, Oxford, Ohio in 2005.He has worked at the Miami University and the Kao Laboratory in Ohio since graduation and is currently working at the Institute of Health and Community Medicine at UNIMAS in surveillance of human Enterovirus as well zoonotic and emerging infectious diseases.

Date: 18th July 2009

Time: 2-4pm (2-2.30pm registration)

Venue: New World Suite 3, Level 5

Free Admission.


Tuesday, June 30, 2009

Alfred Wallace


Forgotten evolutionist lives in Darwin's shadow

- AP Environmental Writer

SANTUBONG, Malaysia -- As he trudges past chest-high ferns and butterflies the size of saucers, George Beccaloni scours a jungle hilltop overlooking the South China Sea for signs of a long-forgotten Victorian-era scientist.

He finds what he's looking for: an abandoned, two-story guest house, its doors missing and ceiling caved in.

"Excellent. This is the actual spot," he yells.

It is on this site, in a long-gone thatched hut, that Alfred Russel Wallace is believed to have spent weeks in 1855 writing a seminal paper on the theory of evolution. Yet he is largely unknown outside scientific circles today, overshadowed by Charles Darwin, whom most people credit as the father of a theory that explains the origins of life through how plants and animals evolve.

Now, in the 200th anniversary of Darwin's birth, a growing number of academics and amateur historians are rediscovering Wallace. Their efforts are raising debate over exactly what Wallace contributed to the theory of evolution, and what role, if any, the spiritual world plays in certain aspects of natural selection.

Beccaloni, a 41-year-old British evolutionary biologist with London's Natural History Museum, is on a quest to return Wallace to what he sees as his rightful place in history. He and Fred Langford Edwards, a British artist making an audiovisual project about Wallace, are retracing the scientist's eight-year trip around Southeast Asia.

Unlike Wallace, Darwin spent two decades developing his theory of natural selection and had far more evidence to back it up, as presented in his defining work, "The Origin of Species," published 150 years ago. But Wallace reached the same conclusion before Darwin published his findings, and Beccaloni contends that Wallace deserves equal billing.

"The Darwin industry is what has distorted the whole of history," Beccaloni said. "People have just concentrated on Darwin and his life and work but they fail to see Darwin wasn't alone and he fits into a wider picture."

Wallace, a British beetle and bird collector, set off for Singapore in 1854. Eight years and 14,000 miles (23,000 kilometers) later, he returned to England as one of the most celebrated biologists after Darwin.

Often traveling with a lone assistant and enduring monsoons and malaria, Wallace collected more than 125,000 birds, beetles and other animals. Thousands were new to the West, including one he named Wallace's golden bird wing butterfly. He shot 17 orangutans and shipped their skins back to Britain, became a fan of the durian - a fruit known for its thorns and powerful odor - and admired the moral character and mental capacity of the Dyak people of Borneo.

But his biggest contribution to science was his writings in the Malay archipelago on evolution and natural selection, building on an earlier four-year trek to the Amazon.

In 1855, he laid out the Sarawak law - named after the place he wrote the paper, now a state in modern-day Malaysia - in which he described evolution as a branching tree. His forceful argument in support of evolution came at a time when creationism, or the idea that God created man, was the popular school of thought.

A year later, he proposed what became known as the Wallace Line after traveling to the islands of Bali and Lombok, in what is now Indonesia. He noticed that bird species were different on each island and concluded that a deep water trench created a boundary that separated the animal species of Southeast Asia and Australasia.

Two years after that, Wallace came up with the theory of natural selection - or survival of the fittest - while bedridden with malaria on another nearby island.

His theory was presented together with Darwin's by the Linnean Society of London on July 1, 1858. Upon his return to England in 1862, Wallace found himself welcomed into a select club of scientists that included Darwin, Sir Charles Lyell, Joseph Hooker and Thomas Henry Huxley.

Wallace became one of the most prominent scientists of his day, publishing more than 800 articles and 22 books over the next 50 years. He was a leading voice in an anti-vaccination movement, a proponent of land reform and the father of biogeography, or the study of the geographic distribution of plants and animals.

"He was a person with a remarkable open mind," said Charles H. Smith, a professor and Western Kentucky University librarian who runs a Web site on Wallace. "He had more concern with science as it related to humankind than practically anyone in his time. That is why he was so interested in social issues."

Wallace died in 1913 at the age of 90. Over the years, he slipped into obscurity, joining a long list - British scientist Patrick Matthews and French scientist Jean Baptist LeMarc among them - whose contributions to evolution theory have largely become footnotes.

The soft-spoken, baby-faced Beccaloni became enamored of Wallace as a graduate student studying the evolution of mimicry in butterflies. He took up Wallace's cause in 1999 after stumbling upon his poorly maintained gravestone in Dorset, England.

Calling himself Wallace's Rottweiler, Beccaloni has barnstormed across England to preserve Wallace homes and other sites. He convinced the Natural History Museum in London to buy the scientist's insect collection, correspondence and books from Wallace's two grandsons.

He also runs a Wallace Web site and is helping British standup comedian Bill Bailey plan a routine based on the scientist. Beccaloni's biggest job by far, however, is defending Wallace's legacy.

He and other scholars claim Darwin conspired to ensure his paper was presented with Wallace's to prevent Wallace from getting sole credit. Roy Davies, the author of the "The Darwin Conspiracy," even accuses Darwin of stealing his ideas from Wallace - an allegation dismissed by other Wallace supporters as unsubstantiated.

But Peter Bowler, a Queen's University of Belfast professor who has spent his career studying evolution theory, contends Wallace's achievements have been exaggerated by his supporters.

Wallace did not have the complete theory and nowhere near the evidence Darwin had compiled - and that was needed to win over a skeptical public, Bowler said. Darwin's evidence included fossil records, animal breeding and heredity, while Wallace relied almost exclusively on biogeography.

"How many years would it have taken Wallace to put together the sort of comprehensive account that would have grabbed people's attention the way 'The Origin of Species' did?" Bowler asked. "Without Darwin, I don't think there would have been a great debate about natural selection in the 1860s and 1870s."

Also controversial is Wallace's support of spiritualism, a popular movement that held seances and believed spirits of the dead can communicate with the living. He upset Darwin and damaged his scientific reputation by arguing that the development of the human mind and some bodily attributes were guided by spiritual beings rather than natural selection, Beccaloni acknowledged.

That has turned Wallace into an unlikely hero among some Christian conservatives opposed to the teaching of evolution. He is also used to support intelligent design, the theory that certain features of life forms are so complex that they must have originated from a higher power.

Michael Flannery, the author of the new book "Alfred Russel Wallace's Theory of Intelligent Evolution," argues that Wallace was in many ways "the seminal figure in what we consider the intelligent design movement." The Seattle-based Discovery Institute, the main supporter of the theory, cites Wallace in its promotional material.

Beccaloni groans when the talk turns to Wallace's spiritualism, noting that he wasn't even a Christian. Christian groups are "grasping at straws," he said, and other academics are using spiritualism to diminish his scientific importance. Beccaloni is trying to keep the focus on his earlier scientific discoveries.

In the Malaysian riverside town of Simunjan, Beccaloni was again on the trail of Wallace. Using Wallace's famous travelogue "The Malay Archipelago" as a map of sorts, he followed a rusted railroad track featured in the book, past paddy fields and palm oil plantations, until the road ended in a peat bog.

That's when Beccaloni began noticing chunks of coal sticking out of the dark soil, a telltale sign of coal works that Wallace described in his book. It was here, Beccaloni surmised, that Wallace spent nine months collecting insects, discovering a strange tree-frog and shooting orangutans.

But nobody would know. The site was unmarked.

Friday, June 26, 2009

Wildlife Faces Cancer Threat


Green turtles around the globe are dying from fibropapillomatosis,

a disease that causes tumors on the skin (pictured here) and internal organs.

(Credit: Cynthia Lagueux)

ScienceDaily (June 24, 2009)

While cancer touches the lives of many humans, it is also a major threat to wild animal populations as well, according to a recent study by the Wildlife Conservation Society (WCS).

A newly published paper in the July edition of Nature Reviews Cancercompiles information on cancer in wildlife and suggests that cancer poses a conservation threat to certain species. The WCS authors highlight the critical need to protect both animals and people through increased health monitoring.

"Cancer is one of the leading health concerns for humans, accounting for more than 10 percent of human deaths," said Dr. Denise McAloose, lead author and Chief Pathologist for WCS's Global Health program. "But we now understand that cancer can kill wild animals at similar rates."

In certain situations, cancer threatens the survival of entire species. The Tasmanian devil, the world's largest carnivorous marsupial, is at risk of extinction due to a cancer known as devil facial tumor disease. This form of contagious cancer spreads between individual Tasmanian devils through direct contact (primarily fighting and biting). To save the species from this fatal disease, conservationists are relocating cancer-free Tasmanian devils to geographically isolated areas or zoos.

Many species living within polluted aquatic environments suffer high rates of cancerous tumors, and studies strongly suggest links between wildlife cancers and human pollutants. For example, the study cites the case of beluga whales in the St. Lawrence River system. These whales have an extraordinarily high rate of intestinal cancer, which is their second leading cause of death. One type of pollutant in these waters—polycyclic aromatic hydrocarbons (or PAHs)—is a well-known carcinogen in humans, and PAHs are suspected carcinogens for beluga whales as well. Fish in other industrialized waterways, including brown bullhead catfish and English sole, also exhibit high levels of cancer.

Virus-induced cancers can affect the ability of some wildlife populations to reproduce. Genital tumors in California sea lions on North America's western coast occur at much higher rates than previously documented. Oceanic dolphin species, such as the dusky dolphin and Burmeister's porpoise (both found in the coastal waters of South America), are also showing higher rates of genital carcinomas.

Other virus-induced cancers can affect the feeding ability or eyesight of wildlife. Green sea turtles—a migratory species in oceans across the globe—suffer from fibropapillomatosis, a disease that causes skin and internal organ tumors. A virus is suspected as the cause these tumors, and environmental factors such as human-manufactured carcinogens might exacerbate their severity or prevalence.

Monitoring the health of wildlife can illuminate the causes of cancer in animal populations; thereby, better safeguarding animals and humans against possible disease. Evaluating cancer threats in wildlife populations requires the collaborative efforts of biologists, veterinarians, and pathologists as well as the earnest engagement of governments and international agencies. The paper concludes that more resources are necessary to support wildlife health monitoring.

"Examining the impact of cancer in wildlife, in particular those instances when human activities are identified as the cause, can contribute to more effective conservation and fits within the One World–One Health approach of reducing threats to both human and animal health," said Dr. William Karesh, Vice President and Director of WCS's Global Health Program

Wednesday, June 17, 2009

Natural Science Lecture: Bats: Whispering Shadows In The Evening Sky

Speaker: Mr Belden Giman

Date: 20th June 2009 (Satturday)
Time: 02.00 pm
Venue: New World 3, Level 5.

The Sarawak Planted Forest (pulp and paper) Project (SPFP), Bintulu Division target is to plant the fast growing Acacia mangium species for the supply of pulp and paper industry. Large forested areas of the SPFP are reserved for conservation of flora and fauna in the project. The Conservation Program for the SPFP is based on cooperative studies with local and international experts on biodiversity, conducting biological inventories with
Conservation Program staff, university students and NGOs. The SPFP Conservation program is supporting awareness program for nature and conservation works besides cataloging the species richness of the SPFP, and to develop an effective long-term biodiversity conservation models for the SPFP.

Speaker Profile:
Mr Belden Giman was formerly graduated from University Putra Malaysia Bintulu Campus in 2004 taking a general Forestry courses for 3 years. He has worked with the Conservation department since January 2005 and dedicated most of his hours of work on mammals in the SPFP. His main interest is emphasizing toward the long-term population of mammals and avifauna (birds) in the SPFP. He is currently working as a research partner with UTAR personnel on the Habitat Suitability of Small Carnivores in monoculture plantation. His main research work now is on mammals’ population trends monitoring in plantation by utilizing remote trip camera. As for bat, data and information collection had just started by doing surveys at several caves and sites within the plantation boundary. This talk provides a platform of exposure for exchanging ideas and methodologies with other expertise.

We welcome all who are interested.

Free Admission


Monday, June 15, 2009

New Chemical Element In The Periodic Table

 

ScienceDaily (June 12, 2009) — The element 112, discovered at the GSI Helmholtzzentrum fĂĽr Schwerionenforschung (Centre for Heavy Ion Research) in Darmstadt, has been officially recognized as a new element by the International Union of Pure and Applied Chemistry (IUPAC). IUPAC confirmed the recognition of element 112 in an official letter to the head of the discovering team, Professor Sigurd Hofmann. The letter furthermore asks the discoverers to propose a name for the new element.


 

Their suggestion will be submitted within the next weeks. In about 6 months, after the proposed name has been thoroughly assessed by IUPAC, the element will receive its official name. The new element is approximately 277 times heavier than hydrogen, making it the heaviest element in the periodic table.

“We are delighted that now the sixth element – and thus all of the elements discovered at GSI during the past 30 years – has been officially recognized. During the next few weeks, the scientists of the discovering team will deliberate on a name for the new element”, says Sigurd Hofmann. 21 scientists from Germany, Finland, Russia and Slovakia were involved in the experiments around the discovery of the new element 112.

Already in 1996, Professor Sigurd Hofmann’s international team created the first atom of element 112 with the accelerator at GSI. In 2002, they were able to produce another atom. Subsequent accelerator experiments at the Japanese RIKEN accelerator facility produced more atoms of element 112, unequivocally confirming GSI’s discovery.

To produce element 112 atoms, scientists accelerate charged zinc atoms – zinc ions for short – with the help of the 120 m long particle accelerator at GSI and “fire” them onto a lead target. The zinc and lead nuclei merge in a nuclear fusion to form the nucleus of the new element. Its so-called atomic number 112, hence the provisional name “element 112”, is the sum of the atomic numbers of the two initial elements: zinc has the atomic number 30 and lead the atomic number 82. An element’s atomic number indicates the number of protons in its nucleus. The neutrons that are also located in the nucleus have no effect on the classification of the element. It is the 112 electrons, which orbit the nucleus, that determine the new element’s chemical properties.

Since 1981, GSI accelerator experiments have yielded the discovery of six chemical elements, which carry the atomic numbers 107 to 112. GSI has already named their officially recognized elements 107 to 111: element 107 is called Bohrium, element 108 Hassium, element 109 Meitnerium, element 110 Darmstadtium, and element 111 is named Roentgenium

Wednesday, June 3, 2009

NSSB visit to Bukit Sarang

On 23-24 May 2009 the NSSB members were invited to visit one of the unique conservation area in Sarawak Planted Forest Project area the BUkit Sarang Conservation Area.

Bukit Sarang is a limestone emergence in kakus. It is a small limestone hill full with small caves suitable for swiflet.

A sustainable harvesting of bird's nest has been implemented here. The visit is mainly to create awareness to NSSB members on the biodiversity that can be found around Bukit Sarang itself besides a learning experience on photography, bird watching and frogging at night.

Here are some lovely photos from my own rack during the visit to share with you all. Enjoy it!

A long way up through a cave called Lubang Pakan to reach to the top of Bukit Sarang






About an hour of climbing will brings you to the peak of Bukit Sarang.









At last...a group photo during the final day of the trip.
This is only the first series of the photographic updates during the visit. I will upload another series of photos during the trip after I am done with editing.

Hopefully the next trip will be more exciting and educating!!

Tuesday, May 26, 2009

TB Vaccine Gets Its Groove Back

 

ScienceDaily (May 24, 2009) — A team of Vanderbilt University Medical Center investigators has cracked one of clinical medicine's enduring mysteries – what happened to the tuberculosis vaccine. The once-effective vaccine no longer prevents the bacterial lung infection that kills more than 1.7 million people worldwide each year.


 

Their solution, reported in the journalPLoS One, could lead to an improved TB vaccine and also may offer a novel platform for vaccines against other pathogens.

"Our findings represent nearly a 180-degree reversal from the dogma of the last 60 years – that the TB vaccine stopped working because it became over-attenuated and was too 'wimpy' to be effective," said Douglas Kernodle, M.D., associate professor of Medicine.

Instead, Kernodle and colleagues found that the TB vaccine has acquired some traits that make it less effective in evoking a sustained immune response. When they take away these traits, the TB vaccine induces stronger immune responses in mice.

The current TB vaccine, known as BCG (bacille Calmette-Guérin), has been around since the 1920s. It was made by weakening (attenuating) a strain of bacteria that causes tuberculosis in cows and that genetically is 98 percent identical to the human TB germ.

During the early years of its use, BCG was 80 percent effective against pulmonary TB. But because there were no long-term storage options for bacterial strains until the 1960s, BCG was grown continuously in culture, with "sub-cultures" of the original BCG maintained in laboratories around the world. Over time, BCG changed – the original vaccine ceased to exist and the daughter sub-cultures lost effectiveness against pulmonary TB.

Today, although BCG no longer protects against lung disease, it is still 80 percent effective against "disseminated TB" (TB infection in many parts of the body) in early childhood. Because of this protection, BCG is given annually to 100 million newborns worldwide – not in the United States and a few other countries – and is estimated to prevent about 40,000 cases each year of TB meningitis and other disseminated TB, Kernodle said.

But the question of why BCG lost its effectiveness against pulmonary TB has not been fully investigated. Researchers accepted the notion that as BCG was grown in culture, it changed genetically and became too weak to evoke the kind of immune response needed for protection.

Kernodle and colleagues came to the problem of BCG's poor activity against pulmonary TB from a different angle. They had reported in 2001 that one way TB itself evades the immune system is by producing antioxidants. Since BCG also produces antioxidants, they suggested that removing BCG's antioxidant-producing capacity might improve the vaccine.

"Our idea to take something away from BCG – and therefore theoretically attenuate it even further – was met with a lot of skepticism," Kernodle said. "But we believed our data that we could make BCG more immunogenic and safer."

Two years ago, after the Kernodle group had modified BCG and was beginning to test it for immune responses, researchers at the Institut Pasteur in Paris published a paper describing the genomic evolution of BCG. They found that in addition to containing gene deletions consistent with attenuation of the vaccine, the BCG genome also had regions of gene duplication and increased gene expression. Some of the duplicated and over-expressed genes were for antioxidants already being targeted by the Kernodle group.

It was suddenly obvious what had happened to BCG, Kernodle said.

"It had not become too weak – instead, by making more antioxidants it had become better at suppressing immune responses."

In the current studies, first author Lakshmi Sadagopal, Ph.D., research instructor of Medicine, vaccinated mice with a modified BCG (genetically changed in three ways to reduce or eliminate the production of several antioxidants) and examined the immune response in the days following vaccination and later with a "challenge" dose of BCG.

She found that, compared to BCG, the modified BCG induced greater cytokine (immune regulatory factor) production during the early phase of the immune response, more CD8 cell-killing T cells at the peak of the primary response, and more CD4 helper T cells during the memory phase. Modified BCG also produced greater recall immune responses and was eliminated better by the vaccinated host animal than the parent BCG vaccine, which might correlate with improved safety in humans.

"At each time point of the immune response, the modified BCG vaccine worked better than the parent BCG vaccine," Kernodle said. "By targeting antioxidants that had increased in expression during decades of cultivation, we ended up making BCG more like it was back in the 1920s when it was 80 percent effective against pulmonary TB. We fixed it."

Using modern molecular techniques to reduce the activity of antioxidants below levels in naturally occurring strains, "it should be possible to make it even better than the original BCG," he added.

The Aeras Global TB Vaccine Foundation, supported by the Bill & Melinda Gates Foundation, has already licensed the modification technology developed by Kernodle and colleagues. Aeras is working to make the best possible modified BCG vaccine, and it has built the infrastructure to conduct clinical trials in South Africa, Kenya and India – countries with a high incidence of TB.

Kernodle and colleagues say the results are also encouraging for other vaccine development. Because the modified BCG produces a better immune response profile than existing vaccine technologies, it could be a useful vector for vaccines directed against other pathogens, including HIV and the parasites that cause malaria.

The National Institutes of Health, a VUMC Discovery Award and the Aeras Global TB Vaccine Foundation supported the research. Kernodle is the David E. Rogers Associate Professor of Medicine.


Adapted from materials provided by Vanderbilt University Medical Center.

Monday, May 18, 2009

High Blood Pressure COuld Be Caused BY A Common Virus, Study Suggests

ScienceDaily (May 16, 2009) — A new study suggests for the first time that cytomegalovirus (CMV), a common viral infection affecting between 60 and 99 percent of adults worldwide, is a cause of high blood pressure, a leading risk factor for heart disease, stroke and kidney disease.

Led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and published in the May 15, 2009 issue of PLoS Pathogens, the findings further demonstrate that, when coupled with other risk factors for heart disease, the virus can lead to the development of atherosclerosis, or hardening of the arteries.
"CMV infects humans all over the world," explains co-senior author Clyde Crumpacker, MD, an investigator in the Division of Infectious Diseases at BIDMC and Professor of Medicine at Harvard Medical School. "This new discovery may eventually provide doctors with a whole new approach to treating hypertension, with anti-viral therapies or vaccines becoming part of the prescription."
A member of the herpes virus family, CMV affects all age groups and is the source of congenital infection, mononucleosis, and severe infection in transplant patients. By the age of 40, most adults will have contracted the virus, though many will never exhibit symptoms. Once it has entered the body, CMV is usually there to stay, remaining latent until the immune system is compromised, when it then reemerges.
Previous epidemiological studies had determined that the CMV virus was linked to restenosis in cardiac transplant patients, a situation in which the heart's arteries "reblock." The virus had also been linked to the development of atherosclerosis, the hardening of the heart's arteries. But, in both cases, the mechanism behind these developments remained a mystery. This new study brought together a team of researchers from a variety of disciplines – infectious diseases, cardiology, allergy and pathology – to look more closely at the issue.
"By combining the insights of investigators from different medical disciplines, we were able to measure effects of a viral infection that may have been previously overlooked," explains Crumpacker.
In the first portion of the study, the scientists examined four groups of laboratory mice. Two groups of animals were fed a standard diet and two groups were fed a high cholesterol diet. After a period of four weeks, one standard diet mouse group and one high-cholesterol diet mouse group were infected with the CMV virus.
Six weeks later, the animals' blood pressures were measured by the cardiology team using a small catheter inserted in the mouse carotid artery. Among the mice fed a standard diet, the CMV-infected mice had increased blood pressure compared with the uninfected group. But even more dramatically, 30 percent of the CMV-infected mice that were fed a high-cholesterol diet not only exhibited increased blood pressure, but also showed signs of having developed atherosclerosis.
"This strongly suggests that the CMV infection and the high-cholesterol diet might be working together to cause atherosclerosis," says Crumpacker. In order to find out how and why this was occurring, the investigators went on to conduct a series of cell culture experiments.
Their first analysis demonstrated that CMV stimulated production of three different inflammatory cytokines – IL6, TNF, and MCP1 – in the infected mice, an indication that the virus was causing inflammation to vascular cells and other tissues.
A second analysis found that infection of a mouse kidney cell line with murine CMV led to an increase in expression of the renin enzyme, which has been known to activate the renin-angiotensin system and lead to high blood pressure. Clinical isolates of human CMV in cultured blood vessel cells also produced increased renin expression.
"Viruses have the ability to turn on human genes and, in this case, the CMV virus is enhancing expression of renin, an enzyme directly involved in causing high blood pressure," says Crumpacker. When the scientists inactivated the virus through the use of ultraviolet light, renin expression did not increase, suggesting that actively replicating virus was causing the increase in renin.
In their final experiments, the researchers demonstrated that the protein angiotensin 11 was also increased in response to infection with CMV. "Increased expression of both renin and angiotensin 11 are important factors in hypertension in humans," says Crumpacker. "What our study seems to indicate is that a persistent viral infection in the vessels' endothelial cells is leading to increased expression of inflammatory cytokines, renin and angiotensin 11, which are leading to increased blood pressure."
According to recent figures from the American Heart Association, one in three U.S. adults has high blood pressure, and because there are no known symptoms, nearly one-third of these individuals are unaware of their condition. Often dubbed "the silent killer," uncontrolled high blood pressure can lead to stroke, heart attack, heart failure or kidney failure, notes Crumpacker.
"We found that CMV infection alone led to an increase in high blood pressure, and when combined with a high-cholesterol diet, the infection actually induced atherosclerosis in a mouse aorta," says Crumpacker. "This suggests that further research needs to be directed at viral causes of vascular injury. Some cases of hypertension might be treated or prevented by antiviral therapy or a vaccine against CMV."
This study was funded by grants from the National Heart, Lung and Blood Institute of the National Institutes of Health.
Study co-authors include Jielin Zhang of BIDMC's Division of Infectious Diseases (co-senior author); Jilin Cheng formerly of BIDMC's Division of Infectious Diseases and now at Fudan University, Shanghai, China (first author); Qingen Ke of BIDMC's Division of Cardiology; Zhuang Jin and Haiban Wang of BIDMC's Division of Allergy; Olivier Kocher of BIDMC's Division of Pathology; and James Morgan of Caritas St. Elizabeth's Medical Center, Boston.
Adapted from materials provided by Beth Israel Deaconess Medical Center.