Day 8 on Chemo regime Alimta/Carboplatin and Trial by local Council NSW to end illegal dumping

Day 8 of chemotherapy should see me starting to feel better. Yesterday was the day of feeling like death warmed up! Back ache, bile and metalic taste, nausea, anxiousness, fatigue and unable to sleep longer than a couple of hours at a time. Today after taking medication to fend off most of the above symptoms I am hoping to come good and enjoy the sunshine that has appeared outside! Expected temperature will be 16 degrees celcius and sunny – a perfect Winter day!Monday brought a wonderful surprise for me – my daughter Jo invited me to a high tea at the beautiful Windsor Hotel, Melbourne. I caught the bus that has replaced all trains for 2 weeks while school holidays are on and so that VLine can work on the rail …

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Weekend and visit to oncologist tomorrow!

Yesterday we slept in after a busy week spent mostly in Melbourne. Strange to say, because of this sleep in, last night was a night where I couldn’t really sleep and just laid there until I got up about 5am, made a green tea and turned the computer on.Saturday we went up to Mt Macedon Trading Post/General store/cafe and where we have our post office box for our mail. As it was absolutely freezing when we left here, I put a scarf/gloves/parka/boots on and jumped in the car, when we got up to our gate … there was a family of kangaroos standing in a row watching us, usually the whole family stand there including uncles/aunts … however yesterday there was the …

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Hi World! Lou is back home!

Hi everyone – I am HOME again after 3 days/2 nights stay in hospital at John Fawkner hospital, Melbourne.I am so overwhelmed with all the beautiful caring messages, phone calls, cards etc that I am receiving – I love you all and thank you for being there – your healing strengths give me hope, love and lift up my spirit to keep on fighting this dreaded asbestos cancer – mesothelioma.Tuesday 6 August I was admitted to the hospital in the wonderful chemotherapy ward – 2West. It is amazing to think that most of the staff have been there on my journey since my treatment commenced in 2003 at this hospital. I was lol treated like a STAR from the time that Keith and myself checked into the hospital where a lovely lady Theresa …

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Being alive with mesothelioma and celebrating the birth of a new grandchild!

My daughter Jo gave birth today to a beautiful and healthy little boy! I am going to visit tomorrow and have my first cuddle – so looking forward to doing so.Also today I have turned the corner after 2 weeks since my last 2 lots of chemo my side effects have eased apart from shallow/tight breathing and slight bile/metallic taste so my immune system is now getting strength again and ready to have chemo next Tuesday (gemzar) and Weds overnight in hospital for the cisplatin.10 years ago when I actually started having palliative treatment for mesothelioma I so wanted to be here to see my little grandchildren being born … I am now up to the count of 5! Now my wish is to see every one of them …

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Asbestos – Living with Mesothelioma in Australia Louise (Lou) Williams: Life between chemotherapy! Visit to Melbourne an…

Asbestos – Living with Mesothelioma in Australia Louise (Lou) Williams: Life between chemotherapy! Visit to Melbourne an…: Yesterday I caught the trains to Melbourne (3 trains altogether) and visited my daughter Jo and beautiful little grandkids including little …

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Shining stem cells reveals how our skin is maintained

Aug. 15, 2013 — All organs in our body rely on stem cells in order to maintain their function. The skin is our largest organ and forms a shield against the environment. New research results from BRIC, University of Copenhagen and Cambridge University, challenge current stem cell models and explains how the skin is maintained throughout life.The results have just been published in the journal Cell Stem Cell.New knowledge challenge stem cell modelsThe skin consists of many different cell types, including hair cells, fat- and sweat glands. It protects us against microbial and chemical attacks and forms a waterproof barrier that prevents fluid loss. Associate professor Kim Jensen’ group from BRIC have through mapping of stem cell’s behaviour in the skin found out that the skin uses a unique method to renew itself. Their results challenge the current perception of how our skin is renewed.”Until now, the belief was that the skin’s stem cells were organized in a strict hierarchy with a primitive stem cell type at the top of the hierarchy, and that this cell gave rise to all other cell types of the skin. However, our results show that there are differentiated levels of stem cells and that it is their close micro-environment that determines whether they make hair follicles, fat- or sweat glands, says Kim Jensen.The new research from Kim Jensen completes the stem cell puzzle.”Our data completes what is already known about the skin and its maintenance. Researchers have until now tried to fit their results into the old model for skin maintenance. However, the results give much more meaning when we relate them to the new model that our research proposes, says Kim Jensen.One such example is that it explains the current mystery of how skin cells can divide too much and initiate a skin cancer, without any traces of genetic change in the stem cells believed to maintain the outer layer of the skin. …

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Cell memory mechanism discovered

Aug. 15, 2013 — The cells in our bodies can divide as often as once every 24 hours, creating a new, identical copy. DNA binding proteins called transcription factors are required for maintaining cell identity. They ensure that daughter cells have the same function as their mother cell, so that for example muscle cells can contract or pancreatic cells can produce insulin. However, each time a cell divides the specific binding pattern of the transcription factors is erased and has to be restored in both mother and daughter cells. Previously it was unknown how this process works, but now scientists at Karolinska Institutet have discovered the importance of particular protein rings encircling the DNA and how these function as the cell’s memory.The DNA in human cells is translated into a multitude of proteins required for a cell to function. When, where and how proteins are expressed is determined by regulatory DNA sequences and a group of proteins, known as transcription factors, that bind to these DNA sequences. Each cell type can be distinguished based on its transcription factors, and a cell can in certain cases be directly converted from one type to another, simply by changing the expression of one or more transcription factors. It is critical that the pattern of transcription factor binding in the genome be maintained. During each cell division, the transcription factors are removed from DNA and must find their way back to the right spot after the cell has divided. …

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Protein changes are discovered that control whether a gene functions are discovered

Aug. 6, 2013 — By studying a gene in yeast, a team of scientists has found that modifications to histones — proteins associated with DNA — can control whether or not a gene is allowed to function and may be important in maintaining the genes’ “expression potential” so that future cells behave as their parent cells did. The research was led by Lu Bai, an assistant professor of biochemistry, molecular biology, and physics at Penn State University, in collaboration with David Stillman at the University of Utah. The discovery, which may have implications for the study of diseases such as cancer, will be published in a print edition of the journal Proceedings of the National Academy of Sciences.Share This:Bai explained that gene expression — the process by which certain genes are regulated or turned “on” or “off” — is one of the most fundamental processes in the life of any biological cell. Different programs of gene expression — even when cells have the same DNA — can lead to different cellular behavior and function. For example, even though a human muscle cell and a human nerve cell have identical DNA, they behave and function very differently. Misregulation of gene expression can affect cell fitness and lead to diseases. “Gene expression tends to vary from cell to cell,” Bai said. “Misregulation may happen in a small fraction of cells, and these cells may cause disease later on. Therefore it is important to study gene regulation at the single-cell level.”Using a fluorescent video of cell division, Bai and her team were able to observe how a gene called HO was expressed in single yeast cells over multiple cell divisions. …

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First probable person to person transmission of new bird flu virus in China: But researchers stress H7N9 is not able to spread efficiently between…

Aug. 6, 2013 — The first report of probable person to person transmission of the new avian influenza A (H7N9) virus in Eastern China has just been published.The findings provide the strongest evidence yet of H7N9 transmission between humans, but the authors stress that its ability to transmit itself is “limited and non-sustainable.”Avian influenza A (H7N9) virus was recently identified in Eastern China. As of 30 June 2013, 133 cases have been reported, resulting in 43 deaths.Most cases appear to have visited live poultry markets or had close contact with live poultry 7-10 days before illness onset. Currently no definite evidence indicates sustained human-to-human transmission of the H7N9 virus.The study reports a family cluster of two patients (father and daughter) with H7N9 virus infection in Eastern China in March 2013.The first (index) patient — a 60 year old man — regularly visited a live poultry market and became ill five to six days after his last exposure to poultry. He was admitted to hospital on 11 March.When his symptoms became worse, he was transferred to the hospital’s intensive care unit (ICU) on 15 March. He was transferred to another ICU on March 18 and died of multi-organ failure on 4 May.The second patient, his healthy 32 year old daughter, had no known exposure to live poultry before becoming sick. However, she provided direct and unprotected bedside care for her father in the hospital before his admission to intensive care.She developed symptoms six days after her last contact with her father and was admitted to hospital on 24 March. She was transferred to the ICU on 28 March and died of multi-organ failure on 24 April.Two almost genetically identical virus strains were isolated from each patient, suggesting transmission from father to daughter.Forty-three close contacts of both cases were interviewed by public health officials and tested for influenza virus. Of these, one (a son in law who helped care for the father) had mild illness, but all contacts tested negative for H7N9 infection.Environmental samples from poultry cages, water at two local poultry markets, and swans from the residential area, were also tested. One strain was isolated but was genetically different to the two strains isolated from the patients.The researchers acknowledge some study limitations, but say that the most likely explanation for this family cluster of two cases with H7N9 infection is that the virus “transmitted directly from the index patient to his daughter.” But they stress that “the virus has not gained the ability to transmit itself sustained from person to person efficiently.”They believe that the most likely source of infection for the index case was the live poultry market, and conclude: “To our best knowledge, this is the first report of probable transmissibility of the novel virus person to person with detailed epidemiological, clinical, and virological data. …

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‘Cowcatcher’ enzyme fixes single-strand DNA

July 29, 2013 — Every time one of your cells divides, it exposes its most essential component to great danger: its genome, the sum total of all its genetic information, embodied in the double-stranded helix of DNA. Prior to cell division, this DNA splits into two single strands, each bearing sequences of biochemical bases that form templates for the genomes of the daughter cells. These single strands are particularly vulnerable to assaults by reactive oxygen species — toxic byproducts of respiration — that could cause changes in the genetic information they contain.Left unchecked, such mutations would quickly add up, producing cells riddled with genetic errors — a recipe for DNA-damage linked disorders such as cancer, aging and neurodegenerative diseases. However, through evolution, mammalian cells have developed a way to repair damaged bases in the single-stranded genome. Now University of Texas Medical Branch at Galveston researchers have figured out how this process works, publishing their results this week in the Proceedings of the National Academy of Sciences.To understand the UTMB researchers’ work, it helps to picture DNA strand separation during replication as analogous to the opening of a zipper. As the “zipper” opens, it exposes strings of four uniformly spaced bases attached to each single strand of DNA. Not far behind, each of these strands is straddled by an advancing “replication complex” of proteins busily copying the single strand back into double strand. The single-strand repair problem is located between these new double strands and the opening zipper, where the DNA is most susceptible to damage and removal of a damaged base would cause the strand to break.The UTMB scientists’ work centers on an enzyme called NEIL1, which scientists knew recognized single-stranded DNA and also knew was associated with the replication complex. In a series of in vitro experiments, the researchers determined that NEIL1 actually rides in front of the replication complex, scouting for single-strand DNA damage.”As soon as it encounters the base damage, NEIL1 binds to the damage site and flags it, and replication cannot continue,” said UTMB assistant professor Muralidhar Hegde, the lead author on the paper. “The replication machinery stalls and then regresses, and the two strands come back together which allows repair of the damaged base in duplex DNA, replacing the damaged base with the appropriate normal base.”Then the “DNA zipper” begins opening again.”The replication machinery comes back and it continues,” Hegde said. …

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Stem cell discovery furthers research on cell-based therapy and cancer

July 19, 2013 — Stem-cell researchers at UC San Francisco have found a key role for a protein called BMI1 that may help scientists direct the development of tissues to replace damaged organs in the human body.”Scientists have known that Bmi1 is a central control switch within the adult stem cells of many tissues, including the brain, blood, lung and mammary gland,” said Ophir Klein, MD, PhD, who directs the Craniofacial and Mesenchymal Biology (CMB) Program and serves as chair of the Division of Craniofacial Anomalies at UCSF. “Bmi1 also is a cancer-causing gene that becomes reactivated in cancer cells.”Klein’s research group now has shown that BMI1 plays another role in ensuring that the process of development unfolds normally.The hallmarks of all stem cells are that they are immature, they keep dividing to replenish their numbers almost indefinitely, and they generate new specialized cells to function in the tissues in which they reside, a process called cell differentiation.Pushed in one direction, the BMI1 switch enables normal stem cells to divide and renew their own numbers. Thrown in the other direction, it keeps cell proliferation in check. But now, Klein’s research team has shown that BMI1 also keeps this stock of stem cells from spinning off daughter cells that mature into the wrong type of specialized cell in the wrong place.The new discovery suggests that manipulating BMI1, along with other regulatory molecules, might one day be among the steps included in molecular recipes to turn specialized cell development on and off to create new cell-based treatments for tissues lost to injury, disease or aging, Klein said.The dual role of BMI1 also is intriguing to think about in pathological settings, such as cancer, Klein said. Growing evidence suggests that many cancers are driven by abnormally behaving adult stem cells or by cells that have abnormally acquired stem-cell-like properties. If these cancerous cells could be made to become specialized cells rather than stem cells when they divide, it might slow tumor growth, some cancer researchers believe. Inactivating BMI1 in cancer stem cells might be one strategy, Klein suggested.The study by Klein’s research team is published in the July issue of Nature Cell Biology, and was conducted on adult stem cells found in the large incisors of mice.Klein, a faculty member of the UCSF School of Dentistry, as well as the School of Medicine, studies teeth, intestines and other tissues to understand the biology and molecular mechanisms that regulate stem cells in these organs. Knowledge gained in these studies can further fuel his specific interest in finding new ways to generate replacement tissue to treat conditions such as Crohn’s disease and craniofacial abnormalities — and to grow new teeth.The incisor of the mouse, unlike any human tooth, grows continuously, and is an attractive focus for stem cell research, in Klein’s view. “There is a large population of stem cells, and the way the daughter cells of the stem cells are produced is easy to track — it’s as if they are on a conveyor belt,” he said. Early in life humans possess stem cells that similarly drive tooth development, but they become inactive after our adult teeth are fully formed during early childhood.In the current study, postdoctoral fellows Brian Biehs, PhD, and Jimmy Hu, PhD, determined that there is a group of adult stem cells at the base of the growing mouse incisor and that these stem cells possess active BMI1. …

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Bearing witness to the phenomenon of symmetric cell division

July 18, 2013 — Writing in his journal about the scientists of his era, Henry David Thoreau bemoaned their blindness to significant phenomena: “The question is not what you look at, but what you see.” More than 150 years later, his words still ring true.For more than a century, scientists have been peering through microscopes, carefully watching cells divide. Until now, however, none has actually seen how human cells manage to divide into two equally-sized daughter cells during mitosis.”This is so obvious when you look at it, but no one ever noticed it,” says Whitehead Institute Member Iain Cheeseman, referring to the work of postdoctoral researcher Tomomi Kiyomitsu. “With careful, visual inspection of dividing cells, you see this observation screaming out at you, but no one ever noticed it was there.”Earlier this year, Kiyomitsu, working in Cheeseman’s lab, saw that during the metaphase cell cycle step a dividing cell uses the motor protein dynein and two signals to perfectly align the cell’s mitotic spindle structure in the middle of the cell. The mitotic spindle is composed of thread-like proteins, called microtubules, which extend from one of two spindle poles on either side of the cell to the duplicated chromosomes in the cell’s center. Other microtubules connecting the spindle poles to the cortex — a protein layer lining the cell’s outer membrane — act to pull the spindle poles back and forth within the cell until the spindle and chromosomes align down the center axis of the cell.Kiyomitsu’s latest work focuses on the next step of mitosis, called anaphase, when the microtubules tear the paired chromosomes apart so that one copy of each chromosome ends up in each of the new daughter cells. His findings are published in this week’s issue of the journal Cell.When cells enter the final stage of cell division, the point where the cell membrane pinches together depends on the position of the mitotic spindle. If the position is in the middle of the cell, the cells divide symmetrically. All human cell lines growing in tissue culture dishes, and about 95% of cells in a human being, split evenly, resulting in daughter cells of equal size. If the spindle is off-center, the daughter cells will be sized differently. Although unequal division occurs among stem cells — allowing one daughter cell to remain a stem cell while the other matures into another cell type, such as a skin or muscle cell — the goal of a normal symmetric cell division is to generate identical daughter cells and increase cell number. …

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Spider webs more effective at ensnaring charged insects

July 4, 2013 — Flapping insects build up an electrical charge that may make them more easily snared by spider webs, according to a new study by University of California, Berkeley, biologists.The positive charge on an insect such as a bee or fly attracts the web, which is normally negatively or neutrally charged, increasing the chances that an insect flying by will contact and stick to the web, said UC Berkeley post-doctoral fellow Victor Manuel Ortega-Jimenez.He also suspects that light flexible spider silk, the kind used for make the spirals on top of the stiffer silk that forms the spokes of a web, may have developed because it more easily deforms in the wind and electrostatic charges to aid prey capture.”Electrostatic charges are everywhere, and we propose that this may have driven the evolution of specialized webs,” he said.Ortega-Jimenez, who normally studies hummingbird flight, became interested in spider webs while playing with his four-year-old daughter.”I was playing with my daughter’s magic wand, a toy that produces an electrostatic charge, and I noticed that the positive charge attracted spider webs,” he said. “I then realized that if an insect is positively charged too it could perhaps attract an oppositely charged spider web to affect the capture success of the spider web.”In fact, insects easily develop several hundred volts of positive charge from the friction of wings against air molecules or by contacting a charged surface. This is small compared to the several thousand volts we develop when walking across a rug and which gives us a shock when we touch a doorknob, but is sufficient to allow a bee to electrostatically draw pollen off a flower before landing.To test his spider web hypothesis, Ortega-Jimenez sought out cross-spider (Araneus diadematus) webs along streams in Berkeley and brought them into the lab. He then used an electrostatic generator to charge up dead insects — aphids, fruit flies, green-bottle flies, and honey bees — and drop them into a neutral, grounded web.”Using a high speed camera, you can clearly see the spider web is deforming and touching the insect before it reaches the web,” he said. Insects without a charge did not do this. “You would expect that if the web is charged negatively, the attraction would increase.”Ortega-Jimenez plans to conduct further tests at UC Berkeley to determine whether this effect occurs in the wild, and find out whether static charges on webs attract more dirt and pollen and thus are a major reason orb web weavers rebuild them daily.

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