hb
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Post by hb on Jul 11, 2006 11:36:19 GMT -5
hi david, i totally agree with you ... every project are not as important but are taken and useful money is wasted... moreover, when the information is not shared then that is again an entire loss as the same mistakes can be repeated or the learning or fault finding can't be assessed... I think that many research can also fail for some minor mistakes/error that other scientist could have detected...
I feel that first we should give priority to those program which promises cure / improvement for all types of Muscular dystrophy followed by other... this does not mean that others are not important.... but major funds will be used to benefit the most.
With regard
hb
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hb
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Post by hb on Jul 16, 2006 3:06:08 GMT -5
Hello luis, If was not typhoid fever, it was malaria… I tried and searched a lot but could not get the prescription as the episode happened in far 2001… It was 9th May 2001 when I was diagnosed with Malaria and my pathological finding stated as :
Peripheral Blood smear for M.P. : Malarial parasites present. Gametocytes of P. falciparum seen.
Urine routine :
Albumin ::: Absent
Sugar ::: Absent
Microscopic ::: Plenty sq. epith cells
I do not understand, hence please co-relate clinically… and I hope that those who understand the type of Malaria can also predict the medicine used for treatment.
These medicine MAYBE also responsible for lowering my cpk to 421 u/l which otherwise before and after would normally stay above 2500 u/l.
This is for your information
Regards
hb
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hb
New Member
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Post by hb on Jul 16, 2006 3:10:05 GMT -5
Hi Andy, Since you too are LGMD 2A... what relief do you get on consumption of Salbutamol??? Pls. let me know if it is any useful... thanks
hb
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Post by David Feder on Jul 27, 2006 21:19:26 GMT -5
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hb
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Post by hb on Jul 29, 2006 2:27:07 GMT -5
David : I got the article downloaded... would go through it and see if can clear few of my doubts. .... hb
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Post by David Feder on Jul 29, 2006 13:57:35 GMT -5
Hawking attacks EU stem cell 'fudge' Stephen Hawking have ALS and is professor of Cambridge University in the same position of Isaac Newton education.guardian.co.uk/higher/news/story/0,,1828355,00.html Renowned British scientist Stephen Hawking condemned as a "fudge" the decision by the European Union over the future funding of stem cell research. Prof Hawking's comments follow the compromise reached by the European Council at its meeting in Brussels yesterday. The council decided that money from the EU's £37m science budget could continue to be spent on research into human embryonic stem cells. But it added the condition that no EU cash will be spent on projects in which human embryos are destroyed, which is necessary to harvest stem cells. That caveat was enough for Germany and seven other EU states to drop their call for a complete ban on future funding on stem cell research. Speaking exclusively to EducationGuardian.co.uk after the decision, Prof Hawking, who has motor neurone disease, said: " I hope this fudge will place no practical limits on stem cell research." Prof Hawking, who is Lucasian professor of mathematics at the University of Cambridge, added: "As I understand it, as long as the creation of new stem cell lines is paid for from private funds, or national budgets, EU money can be spent on research using these lines. "We throw away many embryos in IVF and no one objects. Isn't it better to use a few embryos to save lives?" The decision by the EU comes a week after the US president, George Bush, used his veto to scupper a controversial bill that would have lifted a ban on US federal funding for stem cell research. Britain's science minister, Lord Sainsbury, who attended the EU meeting, said afterwards: "In Europe we are moving forward on this front whereas America has taken, as far as the federal government is concerned, a very negative position. "That Europe is moving forward is extremely good." The decision by Mr Bush to use his veto to block future research funding has triggered the likelihood of an increasing brain drain of scientists with an interest in stem cell research, according to the minister. He said: "In this field we have seen US scientists coming to the UK. If the US continues to take this very negative attitude position I think within this field of regenerative medicine we will see scientists come from America and from other parts of the world, who would have gone to America, to the UK instead." |
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Post by David Feder on Jul 29, 2006 13:59:08 GMT -5
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Post by Andy on Jul 31, 2006 15:00:10 GMT -5
Many many thanks for the document David I will read it over the next week or so. I have been in touch with one of the authors of the paper in the past and found her views very interesting into LGMD.
I will let you know my thoughts when i have read through it ...
but many thanks for posting it for us !!!
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hb
New Member
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Post by hb on Aug 8, 2006 5:48:56 GMT -5
Hello david,
From the article supplied by you on lgmd… my confusion about LGMD2A and 2B was not wrong… Since my Muscular Biopsy report suggested that “POSSIBILITY of dysferlinopathy” while my clinical symptoms are CONTRACTURES of muscles like Walking on toes which is a LGMD-2A (Calpain3) phenotype… Also that those who suffer from LGMD2A (Calpain3) can /may have reduced dysferlin and the reciprocal is also true (LGMD2B can have calpain defect/deficiency).
So, considering all these when it comes to conclusion… I took support of the clinical findings which says that toe walking symptom suggests calpain defect …. while walking on heels (TOES WEAK) and loose muscles suggest dysferlinopathy…. I have seen both type of MD but correct diagnosis is lacking in India… Is my approach correct sir?? has any improvement noted with the boy who got the gene therapy??? any news??
Also… Thanks a lot for providing useful information about LGMD… David sir, While me and few others are concerned and concentrating about our type of MD… you are guiding people on all front….your untiring efforts, keeping in mind about each query “specifically” and taking care of everybody on the board is awesome… My regards for satisfying me everytime…
hb
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Post by Andy on Aug 9, 2006 15:22:25 GMT -5
I agree !
Here's hoping one day we'll all be fit enough to pay David a visit and repay his kindness and hard work in spreading information and through it hope to so many of us...
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hb
New Member
Posts: 19
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Post by hb on Aug 12, 2006 4:14:40 GMT -5
definitely andy... keep the spirit.
hb
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Post by David Feder on Aug 13, 2006 16:14:37 GMT -5
Hi Andy and HB: thank you! I don't know how many time I will keep this website and this message board but I can say that this words is a big stimulus to go ahead with this mission.
Hb, I don't have any information about the results of gene therapy trial. The research will keep the information in secret until they complete the trial and get the information of each boy.
David
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Post by David Feder on Aug 22, 2006 19:53:02 GMT -5
Abstracts from 11th International Congress of World Muscle Society - Bruges, Belgium, October 2006
Clinical features of the limb-girdle muscular dystrophy type 2B
T. Takahashi, , M. Aoki, H. Aiba, H. Sato, E. Abe, M. Ito, Y. Onodera, N. Suzuki, M. Tateyama, H. Konno, H. Onodera and Y. Itoyama - Japan
To establish clinical features of the limb-girdle muscular dystrophy type 2B (LGMD2B). The gene dysferlin was identified in 1998 and founded to be mutated in both patients with LGMD2B and Miyoshi myopathy (MM). We have analyzed the dysferlin gene and detected mutations in 30 families with LGMD2B and 41 families with MM. We had revealed that the G3370T mutation was associated with milder forms of MM. We observed 20 Japanese patients with LGMD2B in whom dysferlin mutations were confirmed. Eight patients of them carried the G3370T mutation. All patients were re-examined for this study. We reexamined the history of the onset and progression of the disease. The clinical examination performed included manual muscle testing using the MRC scale and assignment of scales for the proximal limb muscles as proposed by Brooke et al. Most patients had muscle CT scans at some stage of the disease. Serum CK activity was measured. Cardiological and respiratory function was evaluated in most patients. The mean age at onset was 25 ± 7 years. Patients with the G3370T mutation had a significantly later onset (31 ± 8 years), although the mean age at onset of patients without the G3370T mutation was 22 ± 3 years. The first symptoms in most patients were lower limbs weakness. Four patients had noticed calf hypertrophy at presentation occurred. Two patients were able to stand on tiptoe over 17 years after the onset. On average, patients reached stage 5 of arms and shoulders (Cannot raise hands to mouth but can use hands to hold pen or pick up pennies from the table.) at 30 years of disease duration and stage 9 of hips and legs (Is in wheelchair.) at 25 years of disease duration. The proximal muscles in the upper limbs and the flexor ones in the lower limbs were predominant involvement in the manual muscle testing. The CT scans revealed low density change in the gastrocnemius, soleus, hamstrings, and paravertebral muscles in the early stage. Low density abnormalities in the quadriceps and gluteus were observed after 10 years of disease onset. The anterior tibial muscles were involved later. The gracilis and sartorius muscles were preserved after 20 years of disease onset. All muscles replaced by low density tissue after 30 years of disease onset. Very high serum CK levels were present in the early stage and gradually decreased with disease progression. Most patients did not change ejection fraction on echocardiogram, although one patient manifested cardiomyopathy. Vital capacity decreased with disease progression and three patients needed non inventive positive pressure ventilation. The G3370T mutation was also associated with milder forms of LGMD2B. LGMD2B showed the pattern of muscle involvement which was characterized by early involvement of the posterior muscle compartment including distal lower limb. Cardiac function was preserved and respiratory function was disturbed.
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