CLL - Science topic

Measure it using a nano-drop or a bioanalyzer for quality and quantity. If you have a good amount you can clean it one more time. I recommend the Zymo DNA cleaning kit.

Jean-Jacques Pin Thank you very much for your answer. Really helpful. Best Wishes

Dear Uday,

The inductor in the tank stores an energy Ei= LI^2/2 with L is the inductance and I is the current in the inductor while the capacitor stores an energy CV^2/2 with V the voltage across the capacitor and C is its capacitance. If they connected to form a parallel resonance circuit for example, then it is so that the maximum energy in the capacitor will be equal to the maximum energy in the induct. The maximum voltage on the capacitor will be reached when the current in the circuit is equal to zero with the whole energy stored in the capacitor and the inductor is fully discharged. Conversely, the energy will be fully stored in the inductor when the current reaches its maximum value and the capacitor voltage will be zero pointing out that the capacitor is fully discharged. It is so that the energy will will alternate between the two elements similar to pendulum motion with the alternation between the potential and kinetic energy. The potential energy resembles the capacitor energy and the kinetic energy resembles the inductive energy. So, if the capacitor is known and its maximum voltage is known assuming that we charge a capacitor to a voltage V and then connect across it the inductor.

Then if L is known one can get I, the maximum current in the instructor by equating the two energies.

On the other side normally one wants certain resonance frequency f0 from it one can calculate the inductance of the inductor given C such that L=1/ (2pi f)^2 C.

Then one can size the voltage of the capacitor and the current of the inductor. They are required to specify the capacitor and inductor.

If you connect a resistor RL in parallel with the resonance circuit as a load this load current is normally much smaller than inductance current I. It is equal to V/RL.

Best wishes

Leukemia cell lines

This is an interesting topic. Waiting for some more inputs from other researchers. Good luck!

Hi dear Darellynn Oo

I think the following link can help you;

Best and kind regard.

Hello Mr. Keown,

could you write the exact name of cell line and where did you get, please? Also you can check this encyclopedia. https://portals.broadinstitute.org/ccle

Good day!

Dear Wojciech Witarski

I done Fish according my protocol ( metasystem)

but at last when i look slide under the microscope have not get result, I think Dapi didn't paint cells

can you help me?

What can be reason?

What could be the reason that the dipi can not contain cells?

Thanks Norman. I'll definitely have a look at that going forward.

Hi.. Thanks for the reply. I am doing in the same way. actually i need to know the appropriate freezing media for primary CLL cells.

Hi Manel,

many thanks for your nice comments.

Hope all the best for you during working for scientific investigations:)

Kind Regards

Alireza Goodarzi

At patient may harbor the same karyotype but it is common to find some other additional cytogenetic lesions. Furthermore, the TP53 abnormalities (deletion or mutation) become more common at relapsed in particular among fludarabine-refractory patients.

Hi Max

Did you use exactly 100C? because that is still low.

I assume by collector wall you are referring to the cyclone?

Did you check the total concentration of solids you have in liquid. That's another reason why the particles may not reach the product collection tube if the particles do not have enough solids and are low in density. If you have a picture of the spray dryer and the deposit and you can send it to me, I can probably help you further. my email is ali_al-khattawi@outlook.com

Here are a couple of documents that might be helpful for categorical data:

and

Which also lists some references.

Hi Nicholas,

The abs below work fine. You need Fab2 to avoid FcR interaction. You may also consider attaching these abs onto some kind of beads.

#2022-01 Goat F(ab')2 anti-human IgM-UNLB 0.5mg Cambridge Bioscience

#2032-01 Goat F(ab')2 anti-human IgD-UNLB 0.5mg Cambridge Bioscience

good luck,

Serge

As both Daniela and Divaker have said, I have used the kit to great effect as well.  Have you tried increasing the time of transfer to the positive nylon?

As to the cost of the kit, all of the components can be purchased from various companies (Roche sells a nice set of wash and block buffers, we use IDT for the probe and NEB for the enzymes.  Obviously other companies also sell, and you can make a lot of the buffers from scratch as well) that cuts the cost of the protocol significantly.

Thank you Beatrice! I am familiar with the first 2 papers you sugessted but have not tried to contact the authors as yet. I appreciate your suggestions.

after dropping the slide let it dry overnight and then put it for 2-5 min a 3% (para)formaldehyde solution. Then cells are stabilized and the  you may use normal pepsin treatment and cells should be ok.

Also it happens when you change the batch of pepsin  that you have to test for concentration and time of treatment

Hi Nicholas,

I agree with Daniel. I have had first hand experience with lentiviral transduction with primary B cells. They are extremely difficult to transduce. I have had best success with spinoculation followed by incubation at 32C instead of 37C since the virus is more stable at this temperature.

All the best with your experiment!

Thanks,

Siddha

Sent!

Charging (cationic and anionic ) isnt required for the immunoliposome ,But for delivery system by liposome , cationic and anionicis is required.

Finally,

what is your suggestion ,for negative charge protein delivery in to the leukocyte by immunoliposome method.?

I personally would consider any patient with CLL - even patients in complete remission after successful treatmen - immunosuppressed. I have treated numerous CLL patients in complete remission, which had opportunistic infections. In the case of CLL it is difficult to distinguish immunosuppression due to the disease itself form immunosuppression as a consequence of treatment. The type of therapy is an important factor since many treatment options for patients with CLL are accomanied by severe long-term immune defects, e.g. alemtuzumab or fludarabine. The number of prior treatments also matters, of course. The more prior treatments the higher the degree of immunsupression. That said, a paper by Michael Keating (http://www.ncbi.nlm.nih.gov/pubmed/9694704) showed that CLL patients in complete remission after fludarabine mono had only a low risk of infection. Hower, the patients in this study had receive only one line of therapy (fludarabine mono) which is certainly not representative of the everage CLL patient in 2012, who usually had serveral prior lines of treatment with combination immunochemotherapy. Another study with heavily pretreated patients supports this assumption (http://www.ncbi.nlm.nih.gov/pubmed/21670470). I would also be cautious to draw conclusions from surrogate parameters such as lymphocyte counts or in vitro tests on the risk of infections. In fact, the study by Keating showed that there was no reliable correlation between immune parameters and the rate of infections.

In summary, a patient with CLL in complete remission should usually be considered to be immunsuppressed and treated accordingly.