Ya Binti,

Alhamdulillah, in 2 weeks time, you will turn a year old. How fast time flies.

Lately, you have been a hardworking little girl, practising on your steps. You have been able to cruise around since 9 months and last few days seems to be one of the milestone before you are able to walk on your own.

In one occasion, you were holding your bottle of water to your mouth. As you were doing that, you took small, steady steps walking about the distance of 2 floor tiles. Another was holding to the wall, walking up and down the step to and fro the kitchen and the living room. Good job, my dear little girl!

If more practises were donw, you will be able to walk by 1. Insya Allah.

Wassalam

Ya Binti,

The following video shows how you are able to manouvre the toy aeroplane despite your legs have not reached the ground yet, upon proper sitting on it.

Wassalam

How do we programmatically add a Web Part (that has been deployed) to the Web Part Gallery. On SharePoint this is done via the NewDwp.aspx page.

After spending hours trying to figure out various solutions I was getting no where! The problem is that the list you see on the NewDwp.aspx page is not an SPList! Which makes life a bit tough! The other problem is that the .dwp files displayed in there do not exist until you select them and then click "Populate" by which time they are already in the Web Part Gallery.

I believe the NewDwp.aspx page builds the list of Web Parts , available to be added to the Gallery, from the web.config safe control enteries. Once you click "Populate" the page dynamically builds the .dwp file and adds it to the Gallery.

To add the Web Part to the Gallery programmatically you have to do the same i.e.

• Create the .dwp xml dynamically
• Add it to the Web Part Gallery SPList

Finally, here is how to do it:

using (SPWeb _web = site.OpenWeb())
{
CreateDwpFile();
FileInfo f = new FileInfo("myFile.dwp");
FileStream s = f.Open(FileMode.Open, FileAccess.Read);

_web.AllowUnsafeUpdates = true;
site.AllowUnsafeUpdates = true;
SPList _list = _web.Lists["Web Part Gallery"];
SPFolder _root = _list.RootFolder;
SPFile _spFile = _root.Files.Add("ContentEditor.dwp",s);
_spFile.Update();
}

The CreateDwpFile() method dynamically creates the .dwp file. Then open the Web Part Gallery List and the newly created .dwp file and add it to the root folder of the list.

Elizabeth A. V. Jones, Li Yuan, Christine Breant, Ryan J. Watts and Anne Eichmann

Development 135, 2479-2488 (2008 ) doi: 10.1242/dev.014902

Je ne sais pas si vous avez remarqué, je suis très VEGF ces derniers temps. Isoformes et récepteurs et régulation d'expression de gènes à partir de différentes voies de signalisation, etc. Je suis en train de me régaler avec. Aujourd'hui la récolte a été étonnante, après un croisement de mots clés avec la neuropilin 1, NRP1 pour les intimes. Abondante et avec au moins un petit joyau dedans, pour mon tag "twt" :-)

En fait il semble bien que "time is telling", un autre tag à metre en place ? "tit" ? Yep, je vais commencer à l'utiliser à partir de ce post.

Déjà le titre était intéressant (Separating genetic and hemodynamic defects), prometteur ...

Eh bien, j'aurais parié pour génétique (vous vous en doutiez non ?) dans la cas du knockout Nrp1.

Il n'y avait personne avec qui parier alentours, ce qui fait que j'ai loupé une occasion de gagner un pari :-( Enfin, la lecture du papier a été intéressante quand même.

Jones EAV et al. disséquent le phénotype des embryons des souris Nrp1-/- et la contribution de la circulation à l'établissement de ce phénotype.

Ils montrent que l'interruption du flux chez des wt et des Nrp1-/- ne produit pas chez les wt le même phénotype que chez les Nrp1-/- et concluent que tous les aspects du phénotype Nrp1-/- sont présents en absence de flux; ce qui indique que le phénotype est dû à l'absence de la neuropilin 1 et non pas aux défauts de flux observés.

to the phenotype of wild-type no-flow embryos. Thus, all aspects of the Nrp1–/–yolk sac vessel phenotype develop in no-flow culture conditions, indicating that the phenotype is due to loss of Nrp1 function.

Ils montrent également que chez des embryons wt, l'injection d'un anticorps blocant l'interaction avec le VEGF reproduit le phénotype des Nrp1-/-.

However, inhibition of Nrp1 function with a blocking antibody to the VEGF binding domain in wild-type embryos could clearly reproduce the altered vascular geometry observed in Nrp1 knockout yolk sacs, confirming that this aspect of the phenotype was due to loss of Nrp1 function and not to altered blood flow.

Des éléments de réponse très intéressants pour limiter le rôle des actions mécaniques dans la formation du système vasculaire durant le développement.

Targeted inactivation of genes involved in murine cardiovascular development frequently leads to abnormalities in blood flow. As blood fluid dynamics play a crucial role in shaping vessel morphology, the presence of flow defects generally prohibits the precise assignment of the role of the mutated gene product in the vasculature. In this study, we show how to distinguish between genetic defects caused by targeted inactivation of the neuropilin 1 (Nrp1) receptor and hemodynamic defects occurring in homozygous knockout embryos. Our analysis of a Nrp1 null allele bred onto a C57BL/6 background shows that vessel remodeling defects occur concomitantly with the onset of blood flow and cause death of homozygous mutants at E10.5. Using mouse embryo culture, we establish that hemodynamic defects are already present at E8.5 and continuous circulation is never established in homozygous mutants. The geometry of yolk sac blood vessels is altered and remodeling into yolk sac arteries and veins does not occur. To separate flow-induced deficiencies from those caused by the Nrp1 mutation, we arrested blood flow in cultured wild-type and mutant embryos and followed their vascular development. We find that loss of Nrp1 function rather than flow induces the altered geometry of the capillary plexus. Endothelial cell migration, but not replication, is altered in Nrp1 mutants. Gene expression analysis of endothelial cells isolated from freshly dissected wild-type and mutants and after culture in no-flow conditions showed down-regulation of the arterial marker genes connexin 40 and ephrin B2 related to the loss of Nrp1 function. This method allows genetic defects caused by loss-of-function of a gene important for cardiovascular development to be isolated even in the presence of hemodynamic defects.

Smart Growth, the bastard child of controversial and unpopular Democratic Gov. Parris Glendenning, is once again rearing its ugly head under Gov. Martin O'Malley.

O'Malley is working feverishly with his administration to resurrect the failed concept, give it a massive shot of bureaucratic steroids, and put in place a statewide plan to guide future development.

Even though each locality in Maryland already has its own land-use laws in place, Richard Eberhart Hall, Maryland's planning czar, told the Washington Post that the time has come for the state to steer development!

"One of the problems we have had in Maryland is getting the growth to go where we want it to go," Hall, told the Post. "Just because we have mapped smart-growth areas and identified them doesn't mean there is as much growth there as we would like to see."

Using the carrot and stick of tax incentives and all of the powerful bureaucratic machinery of state government, the O'Malley administration will take an aggressive role in "encouraging" some developments and "discouraging" others.

Meanwhile, property owners and developers will be forced to ignore the marketplace or chance a confrontation with O'Malley's latest form of "Central Planning."

No matter how many laws, regulations, taxes or government edicts are already on the books, O'Malley and his one-party rulers seem to spend their lives thinking up and implementing more and more ad infinitum.

What do you think of the Governor's new/old statewide "Smart Growth" initiative?

Copyright © 2008 UnfreeState.com
All rights reserved.

Marius Wernig, Christopher J Lengner, Jacob Hanna, Michael A Lodato, Eveline Steine, Ruth Foreman, Judith Staerk, Styliani Markoulaki & Rudolf Jaenisch

Nature Biotechnology Published online: 1 July 2008 | doi:10.1038/nbt1483

Une amélioration de l'efficacité d'obtention d'iPS fort intéressante, en utilisant l'induction de l'expression des transgènes par la doxocycline.

The study of induced pluripotency is complicated by the need for infection with high-titer retroviral vectors, which results in genetically heterogeneous cell populations. We generated genetically homogeneous 'secondary' somatic cells that carry the reprogramming factors as defined doxycycline (dox)-inducible transgenes. These cells were produced by infecting fibroblasts with dox-inducible lentiviruses, reprogramming by dox addition, selecting induced pluripotent stem cells and producing chimeric mice. Cells derived from these chimeras reprogram upon dox exposure without the need for viral infection with efficiencies 25- to 50-fold greater than those observed using direct infection and drug selection for pluripotency marker reactivation. We demonstrate that (i) various induction levels of the reprogramming factors can induce pluripotency, (ii) the duration of transgene activity directly correlates with reprogramming efficiency, (iii) cells from many somatic tissues can be reprogrammed and (iv) different cell types require different induction levels. This system facilitates the characterization of reprogramming and provides a tool for genetic or chemical screens to enhance reprogramming.