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Tuesday, December 07, 2004

Bush blocks expanded G.I. Bill benefits for reservists 
The Bush administration is holding up a bill that would significantly expand GI bill benefits for reservists who are on continuuous duty for two or more consecutive years.

The bill, entitled The Veterans Benefits Improvement Bill of 2004 would bring reserve component benefits into closer alignment with active duty benefits - a recognition of the greatly expanded role of reserve component forces in the War on Terror.

Among the bill's provisions:

* Increased availabilty of tuition and educational aid, especially for reservists who have served on extended periods of active duty. Currently, reserve component educational benefits under the Montgomery GI Bill are a fraction of those available to active duty troops.

* Exclusion of GI Bill benefits from calculation of income and assets under federal methodology: a measure that would make it easier for veterans to qualify for need-based financial aid for college tuition and living expenses.

• An increase in the amount veterans are eligible to borrow under the GI Bill mortgage guarantee program.

* A provision allowing spouses of mobilized reservists to break leases. Current law allows this provision for the reservists themselves, but did not expand the benefit to immediate family members.

* Increases the amount of time employers must afford mobilized reservists the option of maintaining civilian health care coverage from 18 months to two years.

The bill, S.2486, was passed by Congress and presented to the President on the 29th of November.

The President, who has resisted past attempts to improve health care coverage for reservists, has yet to sign it.

The President has also opposed measures to set the reserve component military retirement age at 55 - the same age as all other federal employees. Currently, active duty soldiers may retire with full benefits after 20 years of service, or as early as age 37. Reserve component personnel must wait until age 60 to collect retirement benefits.

Just wanted to let him know we noticed.

The President has been no friend to the reserve component soldier, so far.

Splash, out

Jason





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a small cut through the chest wall and puts a thin, lighted tube
called a thoracoscope into the chest between two ribs. Thoracoscopy
allows the doctor to look inside the chest and obtain tissue samples.

If the cancer is in the abdomen, the doctor may perform a laparoscopy.
To obtain tissue for examination, the doctor makes a small incision in
the abdomen and inserts a special instrument into the abdominal
cavity. If these procedures do not yield enough tissue, more extensive
diagnostic surgery may be necessary
The mesothelium consists of a single layer of flattened to cuboidal
cells forming the epithelial lining of the serous cavities of the body
including the peritoneal, pericardial and pleural cavities. Deposition
of asbestos fibres in the parenchyma of the lung may result in the
penetration of the visceral pleura from where the fibre can then be
carried to the pleural surface, thus leading to the development of
malignant mesothelial plaques. The processes leading to the
development of peritoneal Mesothelioma remain
unresolved, although it has been proposed that Asbestos fibres from
the lung are transported to the abdomen and associated organs via the
lymphatic system. Additionally, Asbestos fibres may be
deposited in
the gut after ingestion of sputum contaminated with Asbestos fibres.

Pleural contamination with Asbestos or other mineral
fibres has been
shown to cause cancer. Long thin asbestos fibers (blue Asbestos,
amphibole fibers) are more potent carcinogens than "feathery fibers"
(chrysotile or white asbestos fibers).[6] However, there is now
evidence that smaller particles may be more dangerous than the larger
fibers. They remain suspended in the air where they can be inhaled,
and may penetrate more easily and deeper into the lungs. "We probably
will find out a lot more about the health aspects of Asbestos from
[the World Trade Center attack], unfortunately," said Dr. Alan Fein,
chief of pulmonary and critical-care medicine at North Shore-Long
Island Jewish Health System. Dr. Fein has treated several patients for
"World Trade Center syndrome" or respiratory ailments from brief
exposures of only a day or two near the collapsed buildings.

Mesothelioma development
in rats has been demonstrated following intra-pleural inoculation of
phosphorylated chrysotile fibres. It has been suggested that in
humans, transport of fibres to the pleura is critical to the
pathogenesis of mesothelioma. This is supported by the observed
recruitment of significant numbers of macrophages and other cells of
the immune system to localised lesions of accumulated asbestos fibres
in the pleural and peritoneal cavities of rats. These lesions
continued to attract and accumulate macrophages as the disease
progressed, and cellular changes within the lesion culminated in a
morphologically malignant tumour.

Experimental evidence suggests that asbestos acts as a complete
carcinogen with the development of Mesothelioma occurring in
sequential stages of initiation and promotion. The molecular
mechanisms underlying the malignant transformation of normal
mesothelial cells by Asbestos fibres remain
unclear despite the
demonstration of its oncogenic capabilities. However, complete in
vitro transformation of normal human mesothelial cells to malignant
phenotype following exposure to asbestos fibres has not yet been
achieved. In general, asbestos fibres are thought to act through
direct physical interactions with the cells of the mesothelium in
conjunction with indirect effects following interaction with
inflammatory cells such as macrophages.

Analysis of the interactions between Asbestos fibres and DNA has
shown
that phagocytosed fibres are able to make contact with chromosomes,
often adhering to the chromatin fibres or becoming entangled within
the chromosome. This contact between the Asbestos fibre and the
chromosomes or structural proteins of the spindle apparatus can induce
complex abnormalities. The most common abnormality is monosomy of
chromosome 22. Other frequent abnormalities include structural
rearrangement of 1p, 3p, 9p and 6q chromosome arms.
Asbestos has also been shown to mediate the entry of foreign DNA into
target cells. Incorporation of this foreign DNA may lead to mutations
and oncogenesis by several possible mechanisms:

Inactivation of tumor suppressor genes
Activation of oncogenes
Activation of proto-oncogenes due to incorporation of foreign DNA
containing a promoter region
Activation of DNA repair enzymes, which may be prone to error
Activation of telomerase
Prevention of apoptosis
Asbestos fibers have been shown to alter the function and secretory
properties of macrophages, ultimately creating conditions which favour
the development of mesothelioma. Following asbestos phagocytosis,
macrophages generate increased amounts of hydroxyl radicals, which are
normal by-products of cellular anaerobic metabolism. However, these
free radicals are also known clastogenic and membrane-active agents
thought to promote Asbestos carcinogenicity.
These oxidants can
participate in the oncogenic process by directly and indirectly
interacting with DNA, modifying membrane-associated cellular events,
including oncogene activation and perturbation of cellular antioxidant
defences.

Asbestos also may possess
immunosuppressive properties. For example,
chrysotile fibres have been shown to depress the in vitro
proliferation of phytohemagglutinin-stimulated peripheral blood
lymphocytes, suppress natural killer cell lysis and significantly
reduce lymphokine-activated killer cell viability and recovery.
Furthermore, genetic alterations in asbestos-activated macrophages may
result in the release of potent mesothelial cell mitogens such as
platelet-derived growth factor (PDGF) and transforming growth factor
which in turn, may induce the chronic stimulation and proliferation of
mesothelial cells after injury by Asbestos fibres

Incidence
Although reported incidence rates have increased in the past 20 years,
mesothelioma is still a relatively rare cancer. The incidence rate is
approximately one per 1,000,000. The highest incidence is found in
Britain, Australia and Belgium: 30 per 1,000,000 per year.[7] For
comparison, populations with high levels of smoking can have a lung
cancer incidence of over 1,000 per 1,000,000. Incidence of malignant
Mesothelioma currently
ranges from about 7 to 40 per 1,000,000 in industrialized Western
nations, depending on the amount of asbestos exposure of the
populations during the past several decades.[8] It has been estimated
that incidence may have peaked at 15 per 1,000,000 in the United
States in 2004. Incidence is expected to continue increasing in other
parts of the world. Mesothelioma occurs more
often in men than in women and risk increases with age, but this
disease can appear in either men or women at any age. Approximately
one fifth to one third of all mesotheliomas are peritoneal.

Between 1940 and 1979, approximately 27.5 million people were
occupationally exposed to asbestos in the United States [4]. Between
1973 and 1984, there has been a threefold increase in the diagnosis of
pleural Mesothelioma in
Caucasian males. From 1980 to the late 1990s, the death rate from Mesothelioma in the USA
increased from 2,000 per year to 3,000, with men four times more
likely to acquire it than women. These rates may not be accurate,
since it is possible that many cases of Mesothelioma are
misdiagnosed as adenocarcinoma of the lung, which is difficult to
differentiate from mesothelioma.

Risk factors
Working with Asbestos is
the major risk factor for Mesothelioma A history of
Asbestos exposure exists
in almost all cases. However, Mesothelioma has been
reported in some individuals without any known exposure to asbestos.
In rare cases, Mesothelioma has also been
associated with irradiation, intrapleural thorium dioxide
(Thorotrast), and inhalation of other fibrous silicates, such as
erionite.

Asbestos is the name of a
group of minerals that occur naturally as
masses of strong, flexible fibers that can be separated into thin
threads and woven. Asbestos has been widely
used in many industrial
products, including cement, brake linings, roof shingles, flooring
products, textiles, and insulation. If tiny Asbestos particles float
in the air, especially during the manufacturing process, they may be
inhaled or swallowed, and can cause serious health problems. In
addition to Mesothelioma,
exposure to Asbestos
increases the risk of lung cancer, Asbestos (a
noncancerous, chronic lung ailment), and other cancers, such as those
of the larynx and kidney.

The combination of smoking and Asbestos exposure
significantly
increases a person's risk of developing cancer of the airways (lung
cancer, bronchial carcinoma). The Kent brand of cigarettes used
asbestos in its filters for the first few years of production in the
1950s and some cases of Mesothelioma have resulted.
Smoking modern cigarettes does not appear to increase the risk of
mesothelioma.

Some studies suggest that simian virus 40 (SV40) may act as a cofactor
in the development of Mesothelioma
Exposure
Asbestos was known in
antiquity, but it wasn't mined and widely used
commercially until the late 1800s. Its use greatly increased during
World War II. Since the early 1940s, millions of American workers have
been exposed to Asbestos
dust. Initially, the risks associated with
Asbestos exposure were
not publicly known. However, an increased risk
of developing Mesothelioma was later found
among shipyard workers, people who work in asbestos mines and mills,
producers of Asbestos
products, workers in the heating and
construction industries, and other tradespeople. Today, the U.S.
Occupational Safety and Health Administration (OSHA) sets limits for
acceptable levels of Asbestos exposure in the
workplace, and created
guidelines for engineering controls and respirators, protective
clothing, exposure monitoring, hygiene facilities and practices,
warning signs, labeling, recordkeeping, and medical exams. By
contrast, the British Government's Health and Safety Executive (HSE)
states formally that any threshold for Mesothelioma must be at a
very low level and it is widely agreed that if any such threshold does
exist at all, then it cannot currently be quantified. For practical
purposes, therefore, HSE does not assume that any such threshold
exists. People who work with asbestos wear personal protective
equipment to lower their risk of exposure. Recent findings have shown
that a mineral called erionite has been known to cause genetically
pre-dispositioned individuals to have malignant Mesothelioma rates much
higher than those not pre-dispositioned genetically. A study in
Cappadocia, Turkey has shown that 3 villiages in Turkey have death
rates of 51% attributed to erionite related mesothelioma.

Occupational
Exposure to Asbestos
fibres has been recognised as an occupational
health hazard since the early 1900s. Several epidemiological studies
have associated exposure to Asbestos with the
development of lesions
such as Asbestos bodies
in the sputum, pleural plaques, diffuse
pleural thickening, asbestosis, carcinoma of the lung and larynx,
gastrointestinal tumours, and diffuse Mesothelioma of the pleura
and peritoneum.

The documented presence of Asbestos fibres in water
supplies and food
products has fostered concerns about the possible impact of long-term
and, as yet, unknown exposure of the general population to these
fibres. Although many authorities consider brief or transient exposure
to asbestos fibres as inconsequential and an unlikely risk factor,
some epidemiologists claim that there is no risk threshold. Cases of
Mesothelioma have been
found in people whose only exposure was breathing the air through
ventilation systems. Other cases had very minimal (3 months or less)
direct exposure.

Commercial asbestos mining at Wittenoom, Western Australia, occurred
between 1945 and 1966. A cohort study of miners employed at the mine
reported that while no deaths occurred within the first 10 years after
crocidolite exposure, 85 deaths attributable to Mesothelioma had occurred by
1985. By 1994, 539 reported deaths due to mesothelioma had been
reported in Western Australia.

Paraoccupational secondary exposure
Family members and others living with Asbestos workers have an
increased risk of developing Mesothelioma and possibly
other Asbestos related
diseases. This risk may be the result of
exposure to Asbestos dust
brought home on the clothing and hair of
asbestos workers. To reduce the chance of exposing family members to
asbestos fibres, Asbestos
workers are usually required to shower and
change their clothing before leaving the workplace.

Asbestos in buildings
Many building materials used in both public and domestic premises
prior to the banning of Asbestos may contain
asbestos. Those
performing renovation works or DIY activities may expose themselves to
asbestos dust. In the UK use of Chrysotile asbestos was banned at the
end of 1999. Brown and blue Asbestos was banned in the
UK around 1985.
Buildings built or renovated prior to these dates may contain Asbestos
materials.
Environmental exposures
Incidence of mesothelioma had been found to be higher in populations
living near naturally occurring asbestos. For example, in Cappadocia,
Turkey, an unprecedented Mesothelioma epidemic caused
50% of all deaths in three small villages. Initially, this was
attributed to erionite, however, recently, it has been shown that
erionite causes mesothelioma mostly in families with a genetic
predisposition
Treatment of malignant Mesothelioma using
conventional therapies in combination with radiation and or
chemotherapy on stage I or II Mesothelioma have proved on
average 74.6 percent successful in extending the patients life span by
five years or more [commonly known as remission][this percentage may
increases or decrease depending on date of discovery / stage of
malignant development] (Oncology Today, 2009). Treatment course is
primarily determined by the staging or development. This is unlike
traditional treatment such as surgery by itself which has proved only
be 16.3 percent likely to extend a patients life span by five years or
more [commonly known as remission]. Clinical behavior of the
malignancy is affected by several factors including the continuous
mesothelial surface of the pleural cavity which favors local
metastasis via exfoliated cells, invasion to underlying tissue and
other organs within the pleural cavity, and the extremely long latency
period between Asbestos
exposure and development of the disease
 
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