Neurogenetics - Science topic

Duan i have Reward Deficiency Syndrome, which is the name for the hypodopaminergic antecedent (underlying neurobiological chemical imbalance) which is a precursor to addictions, ADHD, & PTSD. And yes, while this is a neurological/physiological issue, it has psychological ramifications. So i have devised RDS psychoeducation to explain the new paradigm and RDS Solution Focused Brief Intervention. The research study participants (i was the original) in the Elle Foundation 100s and 200s series are provided a new lens through which to view their psychopathology. we have a 100% success rate right now with especially challenged case studies, who experienced multiple 12 step treatments and non-integrated comorbid mental health disorder treatment. Using psychiatric and psychological genomics for improved treatment results.

You can use gnomAD (https://gnomad.broadinstitute.org/) to find variants and mutations found in a large dataset of whole exome and whole genome sequencing.

You can search in ClinVar for any variants/mutations with clinical significance (https://www.ncbi.nlm.nih.gov/clinvar/?term=nrcam%5Bgene%5D)

If you systematically change the photoperiod from 12:12 to another photoperiod in certain small increments that can be a useful way to ascertain the impacts of gradual shifts in the day length. Just because certain photoperiods (e.g., 6:18, 24:0, etc.) have been used should not limit you from looking at others. Having said that, you may find it beneficial to include at least one photoperiod that has been included in other studies for comparison purposes. But ultimately, it depends upon your specific hypothesis you want to test.

thanks again for your kind response ... I'm not sure if we should consider this "a great story behind research" (smile) ... maybe it is only a spontaneous question (?)...

Smart Joelle: why do not we just wait for someone with more knowledge or experience to help us with an example or a different opinion? Specific examples may be premature at this point ... on these slippery issues, it is better to go at low speed (smile)...

Thanks for the answer. i will try your suggestion.

If that is the case and epigenetic changes do alter between adjacent brain regions then what might be the consequences to the “certain receptor” of such changes?  and normal physiological functioning? are there any reported cases of such an occurrence in the literature?

Now comes an innovative pre- and post-fMRI analytical technique at an individual level of analysis-functional connectome fingerprinting (Finn et al., 2015) which may document the efficacy of a treatment intervention to reverse an underlying neural substrate to behavioural inhibition (Bellgowan et al., 2015) to prevent development of an internalising disorder. That conceptual model can be applied to other psychiatric disorders as well.

Finn et al., (2015). Functional connectome fingerprinting: identifying individuals using patterns of brain connectivity. Nat. Neurosci. Oct. 12. doi: 10.1038/nn.4135.

You should use Nissl staining for identifying neurons.  H & E will not distinguish cell types. 

When you say "normal" PCR reactions are you referring to RT-PCR or qPCR? When you are trying to compare upregulation or downregulation of a gene using qPCR, whether it be SYBR or TaqMan assay, you do not need 3 ug. You can most certainly use 100 ng.

In my experience though usually when I say I am using "100 ng" I am referring to the input RNA used to make cDNA. As long as you have the same input RNA in your cDNA reaction then you can just use equal volumes for your qPCR reaction. The cDNA kits I have used have things in the buffer that prevent using a nanodrop to read concentration anyways.

If you could provide more specific information about what type of PCR you are doing that would probably get you a better answer.

Thank you for your kind suggestions, Dr Altay. Will surely check the paper out.

I am currently working on how certain genetic predispositions actually affects the events that occurs in between the primary insult and the secondary trauma in brain injury. For example, rs6265 of BDNF has been implicated to negatively affect certain psychiatric conditions. However, not much work has been done in mTBI, especially with regards to its influence on microstructural changes across different time intervals. While working on the DTI results, we realised that some quarter of our patients with vasogenic edema and astrogliosis (evinced in the preliminary results) performing poorly in neurocognitive assessments across the time points in comparison to others from the same mTBI group. We would like to understand why..

(I posted the question in order to encourage people to share their opinions and engage one another in the effort of advancing the limited knowledge on the subject matter.)

Hi Monika,

Blunt end ligations are less efficient in general but they do work if done properly. The key is to dephosphorylate the vector properly by using an alkaline phosphatase enzyme like this: https://www.neb.com/products/m0371-shrimp-alkaline-phosphatase-rsap

It will be much easier ofcourse if you can generate the PCR product with 3' A overhangs. This will allow you to ligate it into a plasmid like pCR2.1 or pGEM-T and then shuttle it from there into p5E-MCS.

Hope everything works well.

Navneet

thanks for valuable informationAli Abdil Razzaq Muhammed Noori Aldallal  sir 

Hi,

There are several mutations linked to FHM. FHM1 has been linked to a mutation in P/Q calcium channels. FHM2 has been linked to a mutation in the Na/K pump. More recently three mutations in the SCN1A gene (encoding for Nav1.1) were identified, and seem to have different effects on the channel function. Whereas Dichgans et al 2005 and Valmolkot et al 2007 studied the effect of those mutation in heterologous systems expressing a mutated SCN5A, in Kahlig et al 2008 (PNAS) the authors describe the of the three identified mutations of the biophysical properties of SCN1A.

If the variants are truly intronic (i.e. not at splice junctions) there isn't going to be a direct effect on the protein.

There may be an indirect, regulatory effect, but that's unlikely to be reliably predictable. Like Pia says you're likely to need to do an experiment.

Maybe Staufen2 is a candidate.

Regards,

Joachim (not an expert)

Many thanks

Hi,

I recently dealt with Bonferroni corrections. Determine the threshold by deviding 0.05 to the number of SNPs or haplotypes (basically to the number of individual ANOVA tests you have performed) you have analized in that study!

Check paper by:

Kazeem GR, Farrall M (2005) Integrating case-control and TDT studies. Ann Hum Genet. 69(Pt 3):329-35. Good luck!

PCR instruments differ in several parameters such as amount of time to go from one temperature to another, and plates could be from different materials (platinum, ..... )

it could be that this new PCR is worse than the one you use before, I would increase anneling and extension times..... , it may help

I would suggest FBAT or PLINK. If you trait is quantitative you can try QTDT.