Documents raise fresh questions about thalidomide criminal trial
” The dark shadow of thalidomide is still with us. The original catastrophe maimed 20,000 babies and killed 80,000… …Now evidence has been uncovered that the pharmaceutical outrage was compounded by a judicial scandal that has suppurated all these years.
Documents recently unearthed by the UK’s Thalidomide Trust will surely stoke fresh controversy about how and why the criminal trial against the drug’s makers ended without a verdict in December 1970.
And more than half a century since the pill’s threat to an embryo was proven, the company that produced the first disaster has continued to sell the drug in parts of Latin America. ”
A Thalidomide survivor’s story, a triumph of the human spirit over adversity
While the battle for the compensation of Thalidomide victims was raging in the 1970s and is still very much in the news today, former Labour MP Jack Ashley asked in a parliamentary debate how Louise, then 11 years old, could look forward to ‘laughing and loving with no hand to hold and no legs to dance on‘.
Louise was born Louise Mason, a victim of the devastating drug Thalidomide. Born without arms and legs, she is the daughter of David Mason, who single-handedly held out against the drug company, the legal establishment and all the other parents of Thalidomide victims in the high-profile fight for proper compensation for the victims.
As she was photographed with her family and appeared on television meeting celebrities during the battle, few people realised that she did not live with her wealthy parents and three siblings at their spacious North London home but was being brought up in an institution, Chailey Heritage in Sussex. In fact, Louise had never gone home from hospital and, for the first five weeks of her life, her mother didn’t even see her.
This is a survivor’s story, a triumph of the human spirit over adversity. Louise married John, a partially sighted man, and had two beautiful children. She was devastated when she discovered that he was having an affair with their carer. She also had to undergo a kidney transplant, the first Thalidomide victim to do so. She has worked, been an active disability rights campaigner and has now found new love, with Darren, a fellow Thalidomide victim who was born without arms.
DRUG JUSTICE – PHARMACEUTICAL COMPANIES SHOULD PAY FOR THEIR MISTAKES
” We are campaigning to have Grunenthal and Sanofi face their obligations and to stop hiding behind the protection of European legislation, face their responsibility and their guilt, and pay adequate compensation to the thousands of victims affected by their drugs.
The drug thalidomide – marketed for pregnant women suffering with morning sickness – was invented and sold by a German pharmaceutical company called Grunenthal between 1957 and 1961. Thalidomide killed most babies in the womb and those who survived are severely injured and disabled. The drug Epilim (Sodium Valproate) was marketed in 1973 as a drug for Epilepsy and to date has affected approx. 20,000 babies in a similar disastrous way.
Grunenthal has never compensated any British thalidomider. We ask that Grunenthal face their responsibility and give financial compensation to thalidomide damaged people in the UK. Grunenthal’s CEO must sit down with the thalidomide representatives and discuss financial compensation not just for the suffering and pain of living with thalidomide but also for the ongoing extra costs of living with the pain caused by thalidomide “.
Images of the campaigners leading the fight to raise awareness of the Thaliomide scandal
2014 BBC documentary telling the little known story of a father’s battle for justice against one of the UK’s largest corporations.
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In the 1960s, the Thalidomide scandal shocked the world and devastated families. Some victims were left to die, while others were shut away from the world. The fight for compensation saw the government and drug-company silence the press, forcing campaigners to use covert and sometimes illegal ways of keeping their battle in the public eye.
Fifty years on from the tragedy, victims, their families and those intimately involved in the campaign, talk about their ten year battle through the courts and how society has treated them through the years.
TAU research pinpoints mechanism causing rare and severe congenital syndrome
Shortly after thalidomide was released to market in the 1950s, a reported 10,000 infants were born with an extreme form of a rare congenital syndrome – phocomelia – which caused death in 50 percent of cases.
Researchers from Tel Aviv University’s Sackler Faculty of Medicine have identified a regulator – microRNA (miRNA) miR-34 family – responsible for the malformation of limbs in phocomelia, pinpointing a specific target for possible future intervention.
The study reflects the role that epigenetic regulation plays in the development of disease. Embryonic development can be caused by a genetic mutation or by turning the genes on or off without any change in the genetic code itself.
2014 Study Abstract
The tumor suppressor protein p53 is a powerful regulator of the embryo’s susceptibility to diverse teratogenic stimuli, functioning both as a teratogenesis inducer and suppressor. However, the targets that p53 engages to fulfill its functions remain largely undefined. We asked whether the microRNA (miRNA) miR-34 family, identified as one of the main targets of p53, mediates its function as a teratogenesis inducer. For this, pregnant ICR-, p53- and miR-34a-deficient mice, as well as rats, were exposed to 5-aza-2′-deoxycytidine (5-aza), a teratogen inducing limb reduction anomalies (LRA) of the hindlimbs in mice and either the hindlimbs or forelimbs in rats. Using hind- and forelimb buds of 5-aza-exposed embryos, we identified that the miR-34 family members are the most upregulated miRNAs in mouse and rat limb buds, with their increase level being significantly higher in limb buds destined for LRA. We showed that p53 mediates the 5-aza-induced miR-34 transcription followed by met proto-oncogene and growth-arrest-specific 1 target suppression in embryonic limb buds. We demonstrated that p53 regulates the teratogenic response to 5-aza acting as a teratogenesis inducer albeit miR-34a deletion does not affect the susceptibility of mice to 5-aza. Overall, our study thoroughly characterizes the expression and regulation of miR-34 family in teratogen-resistant and teratogen-sensitive embryonic structures and discusses the involvement of epigenetic miRNA-mediated pathway(s) in induced teratogenesis.
Exposure to valproate, thalidomide or alcohol during the first trimester of pregnancy may change the ultrastructure of the placenta
Background: Valproate, thalidomide and alcohol (ethanol) exposure during the first trimester of pregnancy is known to cause several developmental disorders. All these teratogens are known to pass the placental barrier and interfere directly with the normal development of the fetus. However, these teratogens also alter the formation and function of the placenta itself which may in turn affect the proper nourishment and development of the fetus. Optimum development of the placenta requires adequate invasion of trophoblast into the maternal uterine tissues. Changes in the migratory behavior of trophoblast by maternal exposure to these teratogens during placentogenesis may therefore alter the structure and function of the placenta.
Methods: In the present study, the effects of sodium valproate, thalidomide and alcohol on the migration of human first trimester trophoblast cell line (HTR-8/SVneo) were examined in vitro. Cells were cultured in the wells of 48-well culture plates as mono or multilayers. Circular patches of cells were removed from the center of the wells by suction, and the migration of cells into the wound was studied using microscopy. Effects of low and high concentrations of valproate, thalidomide and alcohol were examined on the healing of wounds and on the migration rate of cells by determining the wound areas at 0, 3, 6, 12, 24 and 48 h. Effects of drugs and alcohol on the proliferation and the expression levels of integrin subunits beta1 and alpha5 in cells were examined.
Results: The migration rates of trophoblast differed between wounds created in mono and multilayers of cells. Exposure to teratogens altered the migration of trophoblast into mono and multilayer wounds. The effects of valproate, thalidomide and alcohol on the proliferation of cells during the rapid migratory phase were mild. Drug exposure caused significant changes in the expression levels of beta1 and alpha5 integrin subunits.
Conclusion: Results suggest that exposure to valproate, thalidomide or alcohol during the first trimester of pregnancy may change the ultrastructure of the placenta by altering the migration of trophoblast cells and this effect may be mediated by drug- or alcohol-induced changes in the expression levels of beta1 and alpha5 integrin subunits.
Thalidomide victims to share massive settlement after successful class action
Great news: more than one hundred Australians and New Zealanders living with severe physical deformities because of thalidomide will share in an $89 million settlement after a class action ended in Melbourne.
The British multinational owner of the company that distributed the drug in Australia, agreed to the settlement.
The drug Thalidomide is still causing birth defects in Brazil today
A new scientific study seen exclusively by the BBC indicates that the drug Thalidomide is still causing birth defects in Brazil today. It’s been given to people suffering from leprosy to ease some of their symptoms, and some women have taken it unaware of the risks they run when pregnant.
About ten thousand Thalidomide babies were born worldwide until the drug was withdrawn in the early 1960s. But in Brazil the drug was re-licensed in 1965 as a treatment for skin lesions, one of the complications of leprosy. Researchers now say 100 Brazilian children have injuries exactly like those caused by Thalidomide.