Somali Scientists

[Chimera]

Muna Elmi

Researcher at the Institute of Biomedicine, Department of Medical Chemistry and Cell Biology, Sahlgrenska Academy, University of Gothenburg, Sweden.

[Chimera]

Dr Sada Mire - Archaeologist

Sada Mire‘s interests lie in archaeological and anthropological theory and practice, and cultural heritage policy and management, working in the Horn of Africa. -

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Abdi Osman Jama

Jama is the CEO of ISI (Institute for Strategic Initiatives). His areas of interest are in strategic management and technological capabilities for growth and renewal. He has broad experience as an entrepreneur and senior management consultant. He is former CEO of Eactels Ltd. Abdi has managed many global projects that was spread into Europe, Middle East, Africa and USA. He has been lecturer at EVTEK University of Applied Sciences. He has also taught Business & Technology Alignment in the Haaga-Helia Executive MBA program. He has Masters in Industrial Engineering and Management from Helsinki Metropolia University of Applied Sciences. --

Source

[guerilla]

Quackery is on the rise everywhere. I don't know if you've seen it but Dawkins did an excellent documentary on the topic. Here's a

link.

I watched that ages ago, I recall something about the NHS subsidizing loony docs to help cancer patients, might be wrong.

Wonder if there are any Somali physicists at CERN, now that would be impressive. They could explain it all in Somali,

 

"Higgs Boson wuxu yahay....LHC waa machine weyn raadinaya particle yariis.....bla bla"

[Abu-Salman]

Foad Mohamed: Winner of the Outstanding Achievement at A Level award

Grades: 4 x A at A Level

School: Thomas Tallis School in Greenwich

Other: Foad arrived in the UK from Somalia aged nine, having not been taught to read or write. He served as a translator for Somali parents at school. He was chairperson of the school council and captain of the football team.

(http://www.blackeducation.info/awards/our-prizewinners.aspx)

 

 

 

[...]We are pleased to welcome Mr. Foad Mohamed to the Unit. Foad is an undergraduate student studying for his BMBCH medical degree at Pembroke College, and has joined the Magill Group to undertake his Final Honours School research project. Foad is using light microscopy techniques to define molecular heterogeneity in neurons of the external globus pallidus in dopamine-intact and Parkinsonian brains.

(read here)

 

 

 

 

Now Student at Imperial College London, having finished the 1st part or basic sciences years of his medical degree at University of Oxford (last clinical year; training at Chelsea hospital).

Very interesting young man, passionate about brain disease (Parkinson) research but well read too (quantum mechanics ect).

[QansaxMeygaag]

My my, I had never seen a pic of Sada Mire till now; ain't she gorgeous, beauty and brains!

[Tallaabo]

Apophis;862945 wrote:

The NHS subsidises homeopathy which not only absurd but a waste of money.

 

Here's Southampton peeps trying to "overdose" on homeopathy pills

 

Many of those peeps have since died of the drug overdose:(

[Haatu]

When will we see Safferz's mugshot and bio up here?

[STOIC]

 

 

 

Mohamed H. Farah, PhD

Assistant Professor of Neurology

Johns Hopkins University

 

Axonal Regeneration in the Peripheral Nervous System

 

Peripheral nerve damage and diseases are common health problems that often result in long-term functional deficits. Peripheral axons can regenerate and reinnervate target tissue following nerve injury or disease in young rodent animals. However, human axonal regeneration is very slow and both denervated Schwann cells, which provide a permissive micro-environment for regeneration, and target tissues are at risk for undergoing atrophy and death, precluding functional recovery. This situation underscores the critical need for agents that can speed up axonal regeneration to restore function.

 

A prime candidate for enhancing axonal regeneration is inhibition of Beta -Amyloid Cleaving Enzyme (BACE1). We published a paper showing that genetic deletion and pharmacological inhibition of BACE1 markedly accelerate axonal regeneration in the injured peripheral nerves of mice. However, it is unclear how inhibition of BACE1 improves nerve regeneration. We postulate that accelerated nerve regeneration is due to blockade of BACE1 cleavage of two different BACE1 substrates. The two candidate substrates are the amyloid precursor protein (APP) in axons and tumor necrosis factor receptor 1 (TNFR1) on macrophages, which infiltrate injured nerves and clear the inhibitory myelin debris. In the coming years, we will systematically explore genetic manipulations of these two substrates in regard to accelerated axonal regeneration and rapid myelin debris removal seen in BACE1 KO mice.

 

Equally importantly, we are evaluating a new and very attractive therapeutic approach (e.g. pharmacological inhibition of BACE1) to accelerate nerve regeneration in preclinical rodent models. As experimental models, we employ peripheral nerve injury in mice, and toxin-induced peripheral neuropathy in rodent models. We use combined approaches of morphological, electrophysiological and behavioral studies. These studies are highly relevant because faster rate of outgrowth associated with BACE1 inhibition could be useful in speeding nerve regeneration in human conditions.

 

 

Axonal sprouting and regeneration in motor neuron disease models

 

Distal axonal degeneration is a hallmark of motor neuron diseases, and precedes clinical symptoms onset and motor neuron death both in animal models and human patients. Surviving intact motor axons extend axonal sprouts as a compensatory mechanism to denervated muscle areas, suggesting that an early intervention approach might be to enhance axonal sprouting. Recently, we characterized degeneration and regeneration of a pure long motor nerve. This is the lateral thoracic nerve (LTN) that innervates the back muscle, the cutaneus maximus muscle (CMM). The LTN/CMM system is an ideal system to investigate axonal sprouting and means to encourage axonal sprouting in motor neuron disease models. The LTN is comprised of fast-fatigable ??motor fibers and contains some of the shortest (to the high thoracic region) and the longest (to the region at the base of the tail) motor fibers in the rodent body. It innervates the CMM, which contains type II muscle fibers. The FF/type II motor axon/muscle classes are amongst the most vulnerable in the widely used mouse model of amyotrophic lateral sclerosis (ALS), the G93A SOD1 mouse. We plan to test whether genetic reduction and pharmacological inhibition of BACE1 can enhance axonal sprouting in the LTN and reinnervation of the CMM in G93A SOD1 mice at early stages of axoterminal degeneration.

 

http://neuroscience.jhu.edu/MohamedHFarah.php

 

PS I personally know this dude..One of the Smartest Somali scientist at John Hopkins University.Very humble guy!

 

Now this is a Scientist...take notes Haatu....

[Ambassador]

 

list of Somali engineers from Minnesota.