Multiple forms of Altzheimers?


Conceptual theory the adults with that the genetic’s involved in Amyloid processing leaving to a deficiency in SAP could cause lupus fog the efficiency of APP in the amyloid process could cause Alzheimer’s dementia look up the similarity of the processes and be criteria which they announce it pronounce signalling and communication we may find a difference in the overall management of processes I find that the dissimilarity does not denote a familiarity with Alzheimer’s and lupus however I would like to announce and to put forth the scientific question could there be in fact more than one type of Alzheimer’s dementia ?thereby making it hard to diagnose the disease in one person and compare it to another person because of the dissimilarity of the processing which allows the dementia to thrive

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#AtoZika


Needs explanation how there could be a cure for cytomegalovirus not a cure for Zika is it two diseases parallel them selves in microcephaly and somewhat in symptomology ?the advent of the birth defect be similar symptomology be parallels drawn in genetic transference Where are the genetic parallels for syphilis CMV herpes rubella and other microcephaly causing diseases in infants ?for Crispr cas 9 for the genetic scissors to implement strategies of genetic protocol when it comes to the management of healthy systems over disease traits the aspect of the foetus being surgically operated on noninvasively during ultrasound to prevent microcephaly and microencephaly

of sonar of frequencies of electrical impulses of sensors of encephalogram’s to permit function with holograms animation and interfaces of a non invasive computerized neuroscience surgery See Facebook website Chikungunya and now ZIKA in Barbados

https://www.sharecare.com/health/zika-virus/article/zika-virus-update-latest-news

 

http://www.childrenshospital.org/conditions-and-treatments/conditions/microcephaly/symptoms-and-causes

http://www.sciencedirect.com/science/article/pii/S000292970900024X

http://www.nejm.org/doi/10.1056/NEJMoa1600651#t=article

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Diabetes1+2 apoptosis cells


Through polymerization and self assembly The production of insulin within the cell and the utilization of insulin in the glucose transport system to function at a healthy rate through self-assembly and polymerization induce the stem cells to produce insulin add to induce a glucose transport system to be infused with insulin to conduct itself in the nondiabetic fashion

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Gliomas research technique2


Induced apoptosis of the glioma the subsequent inducement of death in cellular techniques of the glioma to prevent it from spreading the subsequent capture of metastasis of the glioma in the brain to prevent it from spreading the subsequent calibration of blood vessels to prevent the blood vessels from Supplying the main tumour and spreading the access to cells be genetics evolved of the molecular biology be supra molecular biology of the glioma with particle physics Overall all techniques of prevention of spreading of the glioma by harvesting technology that involve holographic displays encapturement encasement and dissolving of trace criteria of the glioma trace elements holograms and Nanomedicine

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Gliomas research technique1


The recalibration realignment the restoration and be re-organization by reversal of engineering reverse engineering of glioma be technique of taking apart the disease and restoring it without its dangerous intention or it’s viral load The possibility of reengineering the glioma to be less invasive to have less of a impact on the brain to be manageable by miniaturization by scattering by dispersal by dissolving by dissipation

treatment by immunoglobulin M

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Gliomas research technique


Integration of stem cells with proper medicated techniques with proper preventative techniques of stem cells with proper genetic alterations integration of stem cells with proper anti-bodies chemotherapy drugs at preventative measures to correct the sequences of events which take place in the brain when the glioma is present the integration of stem cells for the prevention of the regrowth of a glioma in the brain CRISPER techniques to minimally invasive surgeries to correct chromosomal alignment and sequences . Treatment with immunoglobulin  M.

https://garyskeete.wordpress.com/?s=Glioblastoma

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Removal of the genetics of a glioma


From the remaining residue of the successful surgery for glioma the removal of the disease part of the brain due to the fact that this can be utilized in the lab to find out the correct genetics the correct epi-genetics The correct sequence is events that lead to the proliferation of the glioma and the effect that it should constitute a growth in the brain the correct genetics the correct sequences the removal of those glioma causation agents and the subsequent repair by stem cell integration as well as self assembly and polymerization after genetic surgery removing the cause and purpose of the glioma.

 

preventable?
Levin VA1.
Author information
1Neuro-Oncology Unit 431, University of Texas, M.D. Anderson Cancer Center, Houston 77230-1402, USA.
Abstract
Gliomas are a family of primary central nervous system tumors of variable malignancy that are derived from supporting glia (astrocytes, oligodendrocytes, ependymal cells) or their progenitors/stem cells. There are two potential strategies to prevention: preventing gliomas from forming and preventing lower-grade gliomas from developing into higher-grade gliomas. Each would lower time-dependent mortality. Each also depends on an understanding of what causes gliomas so that these factors can be modulated. In this presentation, I will discuss primary prevention, chemoprevention, and screening. I will first focus on the known chromosomal, genetic, and protein changes associated with the different histologic varieties of glioma and the environmental, hereditary, and infectious/viral factors that may promote glioma development and malignant progression. I will discuss a number of clinical scenarios that eventuate from the known genetic patterns of these tumors and the changes in genetic patterns that reflect malignant progression. The basic thinking is that if one could prevent specific gene mutations and/or deletions or gains of specific chromosomes that lead to the development of low-grade (WHO 2) gliomas, then theoretically this would reduce the occurrence of high-grade (WHO 3 and 4) gliomas and hence the almost certain death that now is the fate of most patients with these tumors. In the case of de novo WHO 3 and 4 tumors, being able to prevent or counter specific gene mutations and/or the deletion of specific chromosomes would in itself reduce the occurrence of these gliomas and increase survival. Alternatively, a curative treatment for low-grade glioma that prevents these chromosomal/gene changes would prevent some glioblastomas (WHO 4) from forming and would have the same desired effect on survival. Obviously, for the latter to be achieved, we must also be able to diagnose and treat low-grade gliomas earlier.

 

So will be preventable status would be incurred after the surgery to in sure that the gliomas do not regrow the preventable techniques would be incurred of a chromosome level of genetic level to ensure that the genetics would be safe and secure in the future for the plug to stop the proliferation of the glioma

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047463/

Steroids are commonly administered for the control of edema, mass effect, and side effects from therapy to patients with malignant glioma who are receiving radiotherapy and chemotherapy. Here, we report that therapeutic concentrations of dexamethasone (DEX) attenuate cytotoxicity and growth inhibition of human malignant glioma cells induced by exposure to several chemotherapeutics, including ACNU, VM-26, vincristine, cytarabine, metho-trexate, and adriamycin. DEX-mediated cytoprotection is not linked to DEX effects on glioma cell proliferation. However, the cytoprotective effects of DEX appeared to be more prominent in cell lines with wild-type p53 status (n = 2) than in p53 mutant cell lines (n = 3). Further, DEX-mediated rescue from chemotherapy does not directly involve Bcl-2 family proteins since DEX failed to change the expression of Bcl-2 or Bax proteins and since bcl-2 gene transfer-mediated cytoprotection was not redundant with the effects of DEX. DEX thus appears to control a common, bcl-2-independent death pathway in glioma cells that is not limited to specific drug actions. Chemotherapy is usually given as an elective, adjuvant treatment to glioma patients in stable condition who can tolerate steroid withdrawal. To maximize therapeutic I efficacy, steroids should be withdrawn from glioma patients prior to chemotherapy.

© 1997 by the American Academy of Neurology

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