An article from the economist on hype over hope.
THE unrelenting pace of scientific accomplishment often outstrips the progress of moral thought, leaving people struggling to make sense, initially at least, of whether heart transplants are ethical or test-tube babies desirable. Over the past three decades scientists have begun to investigate a branch of medicine that offers astonishing promise—the ability to repair the human body and even grow new organs—but which destroys early-stage embryos to do so. In “The Stem Cell Hope” Alice Park, a science writer at Time magazine, chronicles the scientific, political, ethical and personal struggles of those involved in the work.
Embryonic stem cells are pluripotent: they have the ability to change into any one of the 200-odd types of cell that compose the human body; but they can do so only at a very early stage. Once the bundle has reached more than about 150 cells, they start to specialise. Research into repairing severed spinal cords or growing new hearts has thus needed a supply of stem cells that come from entities that, given a more favourable environment, could instead grow into a baby.
Immediately after the announcement of the birth of Dolly the sheep—the clone of an adult ewe whose mammary cells Ian Wilmut had tricked into behaving like a developing embryo—American scientists were hauled before the nation’s politicians who were uneasy at the implication that people might also be cloned. Concern at the speed of scientific progress had previously stalled publicly funded research into contentious topics, for example, into in vitro fertilisation. But it did not stop the work from taking place: instead the IVF industry blossomed in the private sector, funded by couples desperate for a baby and investors who had spotted a lucrative new market.
That is also what happened with human stem cells. After a protracted struggle over whether to ban research outright—which pitted Nancy Reagan, whose husband suffered from Alzheimer’s disease, against a father who asked George Bush’s advisers, “Which one of my children would you kill?”—Mr Bush blocked the use of government money to fund research on any new human embryonic stem-cell cultures. But research did not halt completely: Geron, a biopharmaceuticals company based in Menlo Park, California, had started “to mop up this orphaned innovation”, as Ms Park puts it, by recruiting researchers whose work brought them into conflict with the funding restrictions.
Meanwhile, in South Korea a maverick scientist claimed not only to have cloned human embryos but also to have created patient-specific cultures that could, in theory, be used to patch up brain damage or grow a kidney. Alas, he was wrong. But a Japanese scientist did manage to persuade adult skin cells to act like stem cells. If it proves possible to scale up his techniques, that would remove the source of the controversy over stem-cell research.
Three months after he took office, Barack Obama lifted restrictions on federal funding for research on new stem-cell cultures, saying that he thought sound science and moral values were consistent with one another. But progress has been slow: the first human trials in America, involving two people with spinal-cord injuries who have been injected with stem cells developed by Geron, are only just under way. The sick children who first inspired scientists to conduct research into stem cells in order to develop treatments that might help them are now young adults. As Ms Park notes, the fight over stem-cell research is not over, and those who might benefit from stem-cell medicine remain in need.
Wednesday, February 1, 2012
Stem Cell Research
An article from the economist which I am to be very interesting.
FOURTEEN years ago James Thomson of the University of Wisconsin isolated stem cells from human embryos. It was an exciting moment. The ability of such cells to morph into any other sort of cell suggested that worn-out or damaged tissues might be repaired, and diseases thus treated—a technique that has come to be known as regenerative medicine. Since then progress has been erratic and (because of the cells’ origins) controversial. But, as two new papers prove, progress there has indeed been.
This week’s Lancet published results from a clinical trial that used embryonic stem cells in people. It follows much disappointment. In November, for example, a company in California cancelled what had been the first trial of human embryonic stem cells, in those with spinal injuries. Steven Schwartz of the University of California, Los Angeles, however, claims some success in treating a different problem: blindness. His research, sponsored by Advanced Cell Technology, a company based in Massachusetts, involved two patients. One has age-related macular degeneration, the main cause of blindness in rich countries. The other suffers from Stargardt’s macular dystrophy, its main cause in children. Dr Schwartz and his team coaxed embryonic stem cells to become retinal pigment epithelium—tissue which supports the rod and cone cells that actually respond to light—then injected 50,000 of them into one eye of each patient, with the hope that they would bolster the natural supply of these cells.
The result was a qualified success. First and foremost, neither patient had an adverse reaction to the transplant—always a risk when foreign tissue is put into someone’s body. Second, though neither had vision restored to any huge degree, each was able, four months after the transplant, to distinguish more letters of the alphabet than they could beforehand.
Whether Dr Schwartz’s technique will prove truly useful remains to be seen. Experimental treatments fail far more often than they succeed. But the second paper, published in Nature by Lawrence Goldstein of the University of California, San Diego, and his colleagues, shows how stem cells can be of use even if they do not lead directly to treatment.
Since 2006 researchers have been able to reprogram adult cells into an embryonic state, using proteins called transcription factors. Though these reprogrammed cells, known as induced pluripotent stem (iPS) cells, might one day be used for treatment, their immediate value is that they are also an excellent way to understand illness. Using them, it is possible to make pure cultures of types of cells that have gone wrong in a body. Crucially, the cultured cells are genetically identical to the diseased ones in the patient.
Dr Goldstein is therefore using iPS cells to try to understand Alzheimer’s disease. The brains of those with advanced Alzheimer’s are characterised by deposits, known as plaques, of a protein-fragment called beta-amyloid, and by tangles of a second protein, called tau. But how these plaques and tangles are related remains unclear. To learn more, Dr Goldstein took tissue from six people: two with familial Alzheimer’s, a rare form caused by a known genetic mutation; two with sporadic Alzheimer’s, whose direct cause is unknown; and two unaffected individuals who acted as controls. He reprogrammed the cells collected into iPS cells, then nudged them to become nerve cells.
In three of the four Alzheimer’s patients these lab-made nerve cells did, indeed, show higher levels of beta-amyloid and tau—and also of another characteristic of the disease, an enzyme called active GSK3-beta. Since he now had the cells in culture, Dr Goldstein could investigate the relationship between the three.
To do so he treated the cultured cells with drugs. He found that a drug which attacked beta-amyloid directly did not lead to lower levels of tau or active GSK3-beta; but a drug which attacked one of beta-amyloid’s precursor molecules did have that effect. That is useful information, for it suggests where a pharmacological assault on the disease might best be directed.
In the short term, at least, iPS-based studies of this sort are likely to yield more scientific value than clinical experiments of the type conducted by Dr Schwartz, even though they are not treatments in themselves. That will, though, require many more pluripotent cells. And at least one firm is selling a way to make billions of iPS cells for just that purpose. Its founder, appropriately, is Dr Thomson.
FOURTEEN years ago James Thomson of the University of Wisconsin isolated stem cells from human embryos. It was an exciting moment. The ability of such cells to morph into any other sort of cell suggested that worn-out or damaged tissues might be repaired, and diseases thus treated—a technique that has come to be known as regenerative medicine. Since then progress has been erratic and (because of the cells’ origins) controversial. But, as two new papers prove, progress there has indeed been.
This week’s Lancet published results from a clinical trial that used embryonic stem cells in people. It follows much disappointment. In November, for example, a company in California cancelled what had been the first trial of human embryonic stem cells, in those with spinal injuries. Steven Schwartz of the University of California, Los Angeles, however, claims some success in treating a different problem: blindness. His research, sponsored by Advanced Cell Technology, a company based in Massachusetts, involved two patients. One has age-related macular degeneration, the main cause of blindness in rich countries. The other suffers from Stargardt’s macular dystrophy, its main cause in children. Dr Schwartz and his team coaxed embryonic stem cells to become retinal pigment epithelium—tissue which supports the rod and cone cells that actually respond to light—then injected 50,000 of them into one eye of each patient, with the hope that they would bolster the natural supply of these cells.
The result was a qualified success. First and foremost, neither patient had an adverse reaction to the transplant—always a risk when foreign tissue is put into someone’s body. Second, though neither had vision restored to any huge degree, each was able, four months after the transplant, to distinguish more letters of the alphabet than they could beforehand.
Whether Dr Schwartz’s technique will prove truly useful remains to be seen. Experimental treatments fail far more often than they succeed. But the second paper, published in Nature by Lawrence Goldstein of the University of California, San Diego, and his colleagues, shows how stem cells can be of use even if they do not lead directly to treatment.
Since 2006 researchers have been able to reprogram adult cells into an embryonic state, using proteins called transcription factors. Though these reprogrammed cells, known as induced pluripotent stem (iPS) cells, might one day be used for treatment, their immediate value is that they are also an excellent way to understand illness. Using them, it is possible to make pure cultures of types of cells that have gone wrong in a body. Crucially, the cultured cells are genetically identical to the diseased ones in the patient.
Dr Goldstein is therefore using iPS cells to try to understand Alzheimer’s disease. The brains of those with advanced Alzheimer’s are characterised by deposits, known as plaques, of a protein-fragment called beta-amyloid, and by tangles of a second protein, called tau. But how these plaques and tangles are related remains unclear. To learn more, Dr Goldstein took tissue from six people: two with familial Alzheimer’s, a rare form caused by a known genetic mutation; two with sporadic Alzheimer’s, whose direct cause is unknown; and two unaffected individuals who acted as controls. He reprogrammed the cells collected into iPS cells, then nudged them to become nerve cells.
In three of the four Alzheimer’s patients these lab-made nerve cells did, indeed, show higher levels of beta-amyloid and tau—and also of another characteristic of the disease, an enzyme called active GSK3-beta. Since he now had the cells in culture, Dr Goldstein could investigate the relationship between the three.
To do so he treated the cultured cells with drugs. He found that a drug which attacked beta-amyloid directly did not lead to lower levels of tau or active GSK3-beta; but a drug which attacked one of beta-amyloid’s precursor molecules did have that effect. That is useful information, for it suggests where a pharmacological assault on the disease might best be directed.
In the short term, at least, iPS-based studies of this sort are likely to yield more scientific value than clinical experiments of the type conducted by Dr Schwartz, even though they are not treatments in themselves. That will, though, require many more pluripotent cells. And at least one firm is selling a way to make billions of iPS cells for just that purpose. Its founder, appropriately, is Dr Thomson.
Tuesday, January 31, 2012
SMRT 3QFY2011
Results released on 31/1/2012
EPS = 2.4 cents
Total Assets = $1,752,459,000
Total Liabilities = $ 971,819,000
NAV = 51.4 cents
Operating Profit = $46,384,000
Train (P/L) = $25,652K
LRT (P/L) = (92K)
Bus (P/L) = (1715K)
Taxi (P/L) = 1060K
Rental (P/L) = $15,625K
Advert (P/L) = $5,618K
Engineering Svc (P/L) = $718K
Investment (P/L) = ($482K)
EPS = 2.4 cents
Total Assets = $1,752,459,000
Total Liabilities = $ 971,819,000
NAV = 51.4 cents
Operating Profit = $46,384,000
Train (P/L) = $25,652K
LRT (P/L) = (92K)
Bus (P/L) = (1715K)
Taxi (P/L) = 1060K
Rental (P/L) = $15,625K
Advert (P/L) = $5,618K
Engineering Svc (P/L) = $718K
Investment (P/L) = ($482K)
Monday, January 30, 2012
SingPost Q3FY2011/2012
Results released on 30/1/2012.
Underlying Profit = $38.9M (decreased by 5% over corr quarter in prev year)
EPS (Q3 FY2011/2012) = 2.2 cents
DPU Q3 FY2011/2012 = 1.25 cents
Net Gearing = 0.75x
EBITDA to Interest Expenses = 17.4x
Net Debt = $232.4M
Borrowing = $505.7M
Cash & Cash Equiv = $273.3M
NAV (as at 31th Dec 2011) = 16.31 cents
Domestic Mail = $60.3M
Int Mail = $31.8M
Hybrid Mail = $4.9M
Philatelic = $1.0M
Underlying Profit = $38.9M (decreased by 5% over corr quarter in prev year)
EPS (Q3 FY2011/2012) = 2.2 cents
DPU Q3 FY2011/2012 = 1.25 cents
Net Gearing = 0.75x
EBITDA to Interest Expenses = 17.4x
Net Debt = $232.4M
Borrowing = $505.7M
Cash & Cash Equiv = $273.3M
NAV (as at 31th Dec 2011) = 16.31 cents
Domestic Mail = $60.3M
Int Mail = $31.8M
Hybrid Mail = $4.9M
Philatelic = $1.0M
StarHillGlobal Q4FY2011
Results released on 30/1/2012.
DPU for Q4FY2011 = 1.01 cents
DPU for FY2011 = 4.12 cents
Gearing = 30.8%
Interest Cover = 4.4x
Average Interest Rate = 3.25%
Fixed Rate Debt = 87%
Avg Weight Debt Maturity = 2.2 years
NAV (Dec 31th 2011) = 0.95
Total Liabilities = $988,112,000
Net Assets = $1,850,967,000
Total Assets = $2,839,079,000
Major Debt refinancing in 2013.
DPU for Q4FY2011 = 1.01 cents
DPU for FY2011 = 4.12 cents
Gearing = 30.8%
Interest Cover = 4.4x
Average Interest Rate = 3.25%
Fixed Rate Debt = 87%
Avg Weight Debt Maturity = 2.2 years
NAV (Dec 31th 2011) = 0.95
Total Liabilities = $988,112,000
Net Assets = $1,850,967,000
Total Assets = $2,839,079,000
Major Debt refinancing in 2013.
Thursday, January 26, 2012
Ascendas India Trust 3Q FY11/12
Results for 3Q FY2011/2012 released on 26th Jan 2012
3Q FY2011/2012 DPU = 1.5 cents
YTD FY2011/2012 DPU = 4.54 cents
NAV (as at 31th Dec 2011) = $0.7 (compare to $0.8 as at March 2011)
Interest Cover = 3.8
Gearing = 24.6 %
Effective Weighted Avg Cost Of Debt = 6.0 %
Total Assets = $992,962,000
Total Liability = $416,513,000
Net Assets = $576,449,000
largest customer form 6.8% of portfolio base rent!
*SGD appreciated by 16% over the INR over the last one year. Currently at S$1 to INR 40.
3Q FY2011/2012 DPU = 1.5 cents
YTD FY2011/2012 DPU = 4.54 cents
NAV (as at 31th Dec 2011) = $0.7 (compare to $0.8 as at March 2011)
Interest Cover = 3.8
Gearing = 24.6 %
Effective Weighted Avg Cost Of Debt = 6.0 %
Total Assets = $992,962,000
Total Liability = $416,513,000
Net Assets = $576,449,000
largest customer form 6.8% of portfolio base rent!
*SGD appreciated by 16% over the INR over the last one year. Currently at S$1 to INR 40.
First Reit 4Q2011
Results for Q4FY2011 & FY2011 released on 26/1/2012.
NAV (as at 31th 2011) = 80.5 cents
DPU (Q4FY2011) = 1.93 cents
Annualized DPU = 7.01 cents
Total Assets = $660,616,000
Total Liability = $155,317,000
Total Debt = $98,700,000 (from $57,700,000 in Dec 31th 2010)
Interest Cover = 12.3 (from 11.6 in Dec 31th 2010)
Debt-to-Property Ratio = 16% (from 9.4% in Dec 31th 2010)
Rentals from Singapore and Indonesian properties are denominated in Sing dollars whereas rental from Korean property denominated in US dollars
I expect to receive $656.20 in dividend froom First Reit in Feb 2012
NAV (as at 31th 2011) = 80.5 cents
DPU (Q4FY2011) = 1.93 cents
Annualized DPU = 7.01 cents
Total Assets = $660,616,000
Total Liability = $155,317,000
Total Debt = $98,700,000 (from $57,700,000 in Dec 31th 2010)
Interest Cover = 12.3 (from 11.6 in Dec 31th 2010)
Debt-to-Property Ratio = 16% (from 9.4% in Dec 31th 2010)
Rentals from Singapore and Indonesian properties are denominated in Sing dollars whereas rental from Korean property denominated in US dollars
I expect to receive $656.20 in dividend froom First Reit in Feb 2012
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