For the genome end user, I recommend
What a powerhouse of talent. Superb.
More creative juices than a week of summer on a beach.!
So the genome end user is wishing for oncogene specific’s?
here is the frame derived for meiosarcoma.
Retrospective cobalt frame to oncogene specific residue.
*test your residue for challenge in alignment.
*proposed useful towards Harvard large set.
May provide therapeutic avenue.
I cannot resist:
The premise of oocyte external valene determinant upon cell spindle conformational chemistry in trisomy at index case presentation.
by Mark McGary 6/2/14
The valene stack method as a conditional assay in species protein residue has produced exceptional assay fundamental in chromosome of homo sapiens. As a model, it was origined in the CNS gene elements of tissue.
The regard for index case in trisomy, an underlying concern. However, the case presentation as stastastically regarded, demonstrates a certain intersection in protein residue to be adequately modeled. Provision of single point mutation, SNP, mechanism one by one or in the wider sense of chromosomal base (ORF) as intersection lends itself as model, to underlying algorythmic process as blast result. The model conditioned as valene selected, premised to produce trisomy as outcome. An outcome to mutation adventure induced by pathogen residue in a wide assortment or narrow, as the alignments are observed.. I cite the pox virus in insult to reptile as an example. Tryponosome s, limited to the gut of ruminant, appears as a motief within the pox residue, suggesting a cross species insult at predation. (unpublished data).
The models of typicial end user, do not well select for small interior mechanism. This is not to say the pictographs are excellent and superb. Typical blast outcome the engine of all protein specifics. However, the nomenclature as assigned is confusing non protein. Thus, this model will rely upon the protein and molecular weight, deterministic to membrane condition and active stochastically competent model, to more determine the craft and selective regard for mutation adventure as conserved. In this modeling process, outliers are rejected easily. This is not observed within the models of 2007 as shown in non protein relief. See EMBO studies. 2005-present.
In initial model, I was quite surprised at the eucaryotic residue appearance, having expected viral origin. However, I have rather regarded viral -eucaroytic function to appear as residue specific, and exploit whatever such regards are observed in output. This relief, actual, is the model mechanism to output and observation, rather than premised insult. That is to say, observe and follow actual data.
Let us consider the intra uterine enviromental regards. Here we have the tissue and heme supply mechanism to produce a viable embryo, cell mieosis post fertilization, to term. Typically supplying all regards of protection to enable viability. In trisomy, an end process is observed impacted. Mutation adventure, conserved.
Let us grapple with the proceeding of actual trisomy as the index case, and supply effective model to deterministic endpoint. Why valene is useful is observed in the immune challenge of leishmanasis to human host. Here, I draw upon my back ground within infectious disease study to observe the fluke evasion within immune response as mechanistic. All while remembering a key issue. That maternal envelope provides immune response as latent to development in fetal form. Also, is a placental barrier not well exploited by pathogen.
As I observed initial blast determinants, I found that the blast alogrythmic envelope was specific to valene conservation within a set where alogrythm failed at 50% search particulars beyond a slender marginal alignment pathway across species. This suggest a natural limiting outcome, and is premised a superb interior view to both SNP and cognatively small impact sites in chromosome. What was of particular interest in the outcome, was that initial search positional motief regarded chromosome 4, and 21.q22 was observation up codon or yet product undescribed, and actual products were not yet conditions. Hence a regard for low number chromosome as per conditon to trisomy, with valene occurance post meiosis, impacting the developmental initial cycle, was suggested immediately. This suggests typical research method, is rather focused upon outcome, rather than index case and the origin of insult as protein derived. Hence, rather looking in the wrong protein relief suggested as initial mechanism. This with the most cursory of deep views or conditions as applied with Selkov toolbar and the valene modifications observed useful.
Let us further contrast the tral push observation as interesting and coherent to the study of trysomy. Outcomes in chrosomosome mutation adventure having developmental and age resultant pathogenesis.
Here, the goals could be premised as:
1. Continue the valene model to SNP sites and record the set.
2. contrast tral push and Valene block method to 4 site, 21q22.
3. Search for an insult model, with valene precursor as impact and mutation specific.
4. Continue the observation on T vaginalisis as having substance in impact via mole weight particulars observed.
5. Send the best data to membrane at V Cell 5.
The research proceeding for the index case in Downs Syndrome.
The premise of causality in trisomy. By Mark McGary
Having read the overview of studies, spanning a tremendous research effort….I have surmised the defect as causal to chromosome as specific to…..
The drafted gene elements of virus. I will examine this topic, first with brief overviews from within the OMIM entry #190685, assessment page.
*Authors note: Here, the view was later swayed by data to eucaroyte, but impacted also in yersina residues. Hence, indeterminate. But promising in sorting process avaiable.
Warren et al. (1987) and Sherman et al. (1991) have described an association between trisomy 21 and reduced recombination in meioses. A significant proportion (at least 30%) of maternal meiosis I nondisjunctions of chromosome 21 is associated with failure to recombine. It is not known whether the paucity of recombination is related to maternal age; moreover, the mechanism of recombination failure (asynapsis vs abnormalities during or after synapsis) is as yet unclear.
EMBO work superb, but impacted by confusing nomenclature. Huge sets of indeterminate multiple reactions. Not well defined. Premised working with post insult data. This would not well condition underlying mutation.
Why would I grapple with this viewpoint in first intersection? My largest underlying notion to assess syndrome?
Having described the draft element of HIV 1. I would premise a similar conditon towards causal prophensity.
Mapping of the chromosomal region that, if triplicated, results in the phenotypic characteristics of Down syndrome has been facilitated by the use of DNA samples from individuals who have partial trisomy 21 with or without features of the Down syndrome phenotype (Rahmani et al., 1989; 2529205] [Full Text: Elsevier Science]” class=”sectionJump entry-reference” sectionid=”reference49″McCormick et al., 1989; 2143053]” class=”sectionJump entry-reference” sectionid=”reference38″Korenberg et al., 1990; 8055322]” class=”sectionJump entry-reference” sectionid=”reference19″Delabar et al., 1993; Korenberg, 1993). Although detailed analysis of these DNAs is still under way, an area of approximately 5 Mb between loci D21S58 and D21S42 has been identified that is associated with mental retardation and most of the facial features of the syndrome. In particular, a subregion that includes D21S55 and MX1 (interferon-induced protein p78; 147150), the latter being located in band 21q22.3, has been associated with mental retardation and several morphologic features, including oblique eye fissure, epicanthus, flat nasal bridge, protruding tongue, short broad hands, clinodactyly of the fifth finger, gap between first and second toes, hypotonia, short stature, Brushfield spots, and characteristic dermatoglyphics (8055322]” class=”sectionJump entry-reference” sectionid=”reference19″Delabar et al., 1993). Additional phenotypic characteristics may map outside the minimum critical region (symbolized DCR). Material from other rare patients who have features of Down syndrome but no visible chromosomal abnormality may help to narrow down the critical region. In several such studies, however, no triplicated region has been identified (2529205] [Full Text: Elsevier Science]” class=”sectionJump entry-reference” sectionid=”reference49″McCormick et al., 1989; Delabar et al., 1993). It is possible that these patients do not have any chromosome 21 abnormality and their phenotype is a phenocopy of Down syndrome.
after birth. TMD is characterized by an abundance of blasts within peripheral blood and liver, and undergoes spontaneous remission in a majority of cases. TMD may be a precursor to AMKL, with an estimated 30% of TMD patients developing AMKL within 3 years. Mutations in GATA1 are associated with AMKL of Down syndrome. To determine whether the acquisition of GATA1 mutations is a late event restricted to acute leukemia, 12560215] [Full Text: HighWire Press]” class=”sectionJump entry-reference” sectionid=”reference54″Mundschau et al. (2003) analyzed GATA1 in DNA from TMD patients. They found that GATA1 was mutated in the TMD blasts from every infant examined. These results demonstrated that GATA1 is likely to play a critical role in the etiology of TMD, and mutagenesis of GATA1 represents a very early event in myeloid leukemogenesis in Down syndrome. 12586620] [Full Text: HighWire Press]” class=”sectionJump entry-reference” sectionid=”reference33″Hitzler et al. (2003) likewise presented evidence that GATA1 mutations are an early event, and that AMKL arises from latent transient leukemia clones following initial apparent remission. All 7 patients reported by 12560215] [Full Text: HighWire Press]” class=”sectionJump entry-reference” sectionid=”reference54″Mundschau et al. (2003) and almost all of the patients studied by 12586620] [Full Text: HighWire Press]” class=”sectionJump entry-reference” sectionid=”reference33″Hitzler et al. (2003) had deletions or insertions in the GATA1 gene rather than nucleotide substitutions.
12200707] [Full Text: Nature Publishing Group]” class=”sectionJump entry-reference” sectionid=”reference80″Taketani et al. (2002) screened the RUNX1 gene (151385) in 46 Down syndrome patients with hematologic malignancies. They identified a heterozygous missense mutation (H58N; 151385.0008) in 1 patient diagnosed with TMD 5 days after birth. The patient died suddenly 12 months after birth; it was not known whether she developed acute myeloid leukemia.
Here, I confess to having not well noted the source: Above. I hope the interested reader will forive that omission and I will review my notes. Adapting to the internal references cited within the text.
This page is actual research notation, and I hope the research and review inquiry to disease will forgive my oversight if I fail to mention every particular. In typical end use, the data is origined at NIH, NCBI. Chromosome data via OMIM.site.
Here, the coherent observation implied by myeloid descriptors above….should be contrasted with the Tralpush observations available.
Let us examine the viral assignment of residue in HIV -1 as a graphical model. *Viral residues sourced via VIPR, IRD. HIV glycoprotein source. NCBI, NIH
The observation of HIV -1 draft mosaic comes as the residue specifics of homo sapiens, with corresponding blast output….as shown with addative HIV residue…to blast align with the viral residue set. Hiv latency, demonstrated in one model as ocular and CNS site specific, also has interesting interaction with cis and trans affinity to that locus as residue assay proceeds.
Here, I premise a similar mechanism causal to the chromosomal mutation adventure, observed in c21q22.1, 23. Observe the variant other abberant forms and site locus to premise corespondance to my premised mechanism. In fact, a typical post insult viral prophensity. See the Nile crocidile pox virus at insult to crocidilla for an interspecies example.
Multiple studies, have engaged the murine model to demonstrate alteration…… However, I premise skewed results in that small but vital pathway in mouse, the sweet receptor as an exemplar, are in fact missing in the non primate model. I have become rather skeptical of proposed findings in this regard. This research habit to murine model perhaps driven by cost contraints is non determinant in some particulars……and potentially the most vital particular.
The hedgehog would be a much better selection in mammal;, with rabbit an addative species selection. This popularity of murine model driven by cost constraint I premise with sever limitation, and skewed result. Would the interested reader have every mammal challenge working and effected on a mammal lacking the homo sapiens pathways vital to research in the drug formulary applied as intra venous challenge to their own vein? I would think not.
Another strong indication of study regards, the rather high case presentation at live birth. 1 in 1000, a particular cited. Clearly, a potential for conserved mutation adventure could be postulated in population observed to potential for viral insult.
Therefore, using a particular toolbar modified to acertain v-117 non polar mole weight affinity in residue endpoint, hence to assigned reassortment, a deterministic set of output can be surmised. My task now become organ and species specific.
That data: below.
Preliminary data in research notebook, of first output via Selkov 117 modification.
Yet to be fully engaged. Initial sets and research topics are briefly surmised in attachments, per UDP assingment.
Alternate model of trysomy index case in mannose microphage receptor site via bacteriacemic insult pre-ovary production of oocyte.
Here, the avenue of study, shifting from the view of viral residue to mannose receptor. An excellent 1990 Harvard study described the implication in ovary. Thus, the research direction here has strong implied reproductive impact as research arm.
Interestingly, the process of elimination could be well served by clinicial trial in the modern test output and sample available. However, I consider my assay skills adequate to narrow the particulars of this interesting study.
This refinement in view now can be contrasting data as re examined for best particular protein for study. Having long engaged in research, I do feel the mannose has the right sensibility. Why.
Becase of the documentaion included in the 1990 Harvard paper.
The particulars of alignment are tremendous:
YP_003965969 —————————————————————————- ADU56613 1 PALCFVVPDGYK-FTGNVLILLECFVRSSPVNFEQKYLEDYKKLEQLKGDLE—SVGINLVPLIDGRTTFYNEQI 152 XP_004716076 1 MPLPFSVKVWEQdLRGRSLIFEIRDISHSPIEQQHHLLTPPGETVHCASDLRtilSVIQYEYYLPSAQSVSRNESA 76 YP_003965969 ——————————————————————————– ADU56613 153 PDWVNDKLRDTLFALLKYSQESNALFEESEYSRLCESLALTSGRLSGIESINALIDNR–ARHFEELISCCHQGINNKLS 230 XP_004716076 77 AETLTERHPVVVESILTPEDALRSESEETWAPRALNALGPGQPLDRQTFALRRLTDTRqfLIYNEDHKRCVEVVDAGAVQ 156 YP_003965969 ——————————————————————————– ADU56613 231 AHDVKSSIEEEYQIFRNKLRQGGIESQFIKTDKVKLLEDFRNLYNDKISTHDESIEQLTFQFQRASPVLKFLYADLNSSE 310 XP_004716076 157 TAVCNPDSESQKFRWVSDYHLMSVALKLCLGVPSKTDWVKVLLYACENSKEDQKWECKNDTLFGLRGEELYFNYGNRQEK 236 YP_003965969 —————– ———————————————————— ADU56613 311 EKPVDPQNGQMQCWRSF LNKVKSLRILNTRRKLLLVFDVLILLASRLDCLEHNNKYLVGWLGSCFVSVNDRLVSLES 387 XP_004716076 237 NIMLYKGSGLWSRWKIYRGYEAMFTLLGNANGATCAFPFKFENKWYADCTSAGRSDGWLWCGTTTDYDTDKLFGFCP 321 YP_003965969 ———- ——————————————————– —— ADU56613 388 TK-RDLKR-WNHELLTIIN-KVLTRATNALKEVGIEIDSYGIDLKILDCDVYDTIMSIEVSGVTPTYTLGVV 489 XP_004716076 322 MKfEDSERlW NKDPLTSISyQINSKSALTWHQARKSCQQQNAELLSITEVHEQTYLTGLTHALTSG LWIGLN 393 YP_003965969 —————————————————————— ———– ADU56613 490 DILNATDLERLSTLSLALINSMKTSSTVKLRQN–EFGPSRYQVVRCKEAYCQEFFVNKIGFKLLY QKTGECSKCYA 564 XP_004716076 394 SLSFNTGWQWSNRSPFRYLNWLPGSPSTEPGKScvSLNPGKNAKWENLECIQKLGYICKKGNSTLNSESDVPTSCPS 475 YP_003965969 ————————————————– ————————— ADU56613 565 INNNVVGEVCSFYADPKRFFPAVFSSDVLQKVVNVMVSWIEECSELSEQL VTIKLLTKMILVLILTHPSKRCQKFLQ 641 XP_004716076 476 QWWPYAGYCYKIHRGAKKIQRDALTACRKEGGDLASIHSIEEFDFIFSQLDELWIGLNDINIQMYFEWSDRTPVTFT 557 YP_003965969 ——————————————————————————– ADU56613 642 NIRYFVMAFVSDFHHKDLIDKIREDLITEVEY-LLYKLVCHLLGIILSEEVVSMMTNRFKFVLNISYMCHFITKETPDRL 720 XP_004716076 558 KWLRGEPTHENYRQEDCVVMKGKDGYWADLACeQPLDYICKMKSQSQAPEIVEVETGCRKGWKKHGFYCYLIGHTLSTFT 637 YP_003965969 1 ——— —————————————————————–ME 2 ADU56613 721 TDQIKCFEKNPKDDASEEELHEMIYNARKFLSKECCADADKVRYKKPGVSKKFISLLVSSFNNGSLFKGKEVKKAL 809 XP_004716076 638 EANKTCGNE KAYLTTVEDRYEQAFLTSLVGLRPERYFWTGLSDVQSKGTFQWTIGEEVQFTHWNSDMPGRKAGCVA 713 YP_003965969 3 VDFFEQKKQETGVNLSAVQREAVE-HTEG-ALL——-VLASPGSGKTTMMIMKIGYLIEEKDVDPSRIRAVTF—- 69 ADU56613 810 LDPLITSGCATALDLASNKSVVVNKYTDG-SRVLDYDFNKLTALAVTQLTEVFARKGKYLLNKQDYDYKIQQAMSNLVLG 888 XP_004716076 714 MRTGSAGGLWEVLKCEEKVKFVCKHWAEGvTRPPEPTTTPEPRCPENWGTTSHSSLCYKLFTKGKHDKKTWFESRDFCRA 793 YP_003965969 70 SNASATDMDNRFDKLFPHLKDNKVKFSTIHSFAFEVVRAYFKKNNiRYQLIEGNMDKPNSEPCRVVNKLNKRIILRRIFR 149 ADU56613 889 SKEGSSDINNTDLDEILLDGGASEYFDHLRCTVDNIISQYRELPG-RQQQVDCSSPSISDLDKVVEEKLFIRLIKSELSN 967 XP_004716076 794 LGGDLASINHKEEQQA–IWRLITSGSNYHELFWLGLTYASPSEG–FTWSDGSPVSYEHWAFGEPNNYQNTEYCGELKG 869 YP_003965969 150 E—-VTQENVTEEQMEELLSYI—SYIKNKLIPYDQLEDI—ETSIPSASEIFLSYEEFKCADFTNRLVDYDDMLVI 219 ADU56613 968 HmiEDFDRETLPEDQYVKICESIYGDETLRDKYFYTGPMNSCpigELTKAVVTRTFLDQEYFQCFKSILLVMNGNRLMGK 1047 XP_004716076 870 D–PSMSWNDINCEHLNNWICQIKKGQTLKPEPTPAPQDNPQ——–VTADGWIIYNEQEQYYISKEKENMDNARAF 939 YP_003965969 220 ANDALEKDAGMLAEYQSMFDYFLTDESQDNSLVQNLII —EKLVRLKGNICVVADDDQSIYGWRGAAPEYLLN— 290 ADU56613 1048 YSHYKSKCLNFKFDTGKLADDVRISERESNSEALSKAL SLTNCTTAMLKNLCFYSQESPQSYNSTGPDTGRLKFSLS 1124 XP_004716076 940 CKKNFGDLASIKGESEKKFLWKYVNRNDPQSAYFIGLLKKFSWMDGSKVDFVAWATGEPNFANDDENCVTMYSNSGF 1020 YP_003965969 291 FKEVYPNAKILYMVQNYRSTKDIVEV ANQFIKRNKNRYDKEMFTEKESFKPIQLSHLDTYEAQIRHIVEKVKYAP 365 ADU56613 1125 YKEQVGGNRELYIGDLRTKMFTRLIE -DYFEALTSQLTGSCLNNEKEFDNAILSMKLNVSSAHVSYSMDHSKWGP 1204 XP_004716076 1021 WNDVNCGYPHAFICHRHNSSINSTALIFGFVEDERKNWHEARTACKEFKGNLVSILNEKEQAFLTYSMRGSNFDA 1119 YP_003965969 366 —VKKEVAILYRNNSSSIALIDELE———HQGIPFYI———–KDSDNKFFSHWIIEDILNFMRMSY– 420 ADU56613 1205 FLTIIQNLILLSDDLQADLKGKDYLSTLLTWHMHKMVEIPFNVVSAMMKSYIKSQLGLKKKTTQSVTEDFFNSNFQTGTV 1284 XP_004716076 1120 WIG-LNDVNSEHTFLWTNQRGVHYTNWGKGYPGGRRSSLSYEDADCVVMIGGKSRDA–GQWMDVPCDSKRGYICQAPLV 1196 YP_003965969 421 ——————SDKHPILLEKIHTKFNGYINKPQIEYLKEINNKASVFDNLLK————-LNVPVYQ 469 ADU56613 1285 PSHISSILDMGQGILHNTSDFYALISERFINFAVKCVSGGQIDAYTSSDDQISLFDQNLTQLLSRDEEEFKTLLEFHYYM 1364 XP_004716076 1197 NSLPLPTTSPPEGFINLGADSYSLIKHKYSWF———-EADNNCKNQNSKIGSILDPYSNAFVWLHMQTSNVPVWI 1266 YP_003965969 470 RKNLGKCKE IFKRINQLRPDQaIRVIRDELGYEKKLVKM-CESLGFKK-EYLLSILNTLQGIGSKLETLKDFAERLN 544 ADU56613 1365 SDQLNKFVSIGRFVAEFKSRF-Y-VWGDEVPLLTKFVAAaLHNIKCKEpHQLAETIDTIIDQSVANGVPVDLCNQIQ 1443 XP_004716076 1267 ALNSNLTKN EYAWTDNWRMRY-TNWAADEPKLKSACVY–LDTDG—-YWKTAHCNESLYSLCKRSDDIPATEPPQ 1336 YP_003965969 545 YLRKVLSQ—–SKFEKGKDVVTLSTFHSSKGLEFNQVIMIDLIEGVIPSK-EVIKDFKSGKIDEMEEAvRLFYVGMTR 618 ADU56613 1444 –KRTLSL–LCYAKYPIDPFLLNCETDVRDWVDGNRSYRIMRQIERLVPDAcKKMRSMLRILFNKLKTG-ELHEEFTTN 1518 XP_004716076 1337 LPGRCPESdhTAWIPFHGHCYYIE-SSYTRSWGQASLECLRMGSTLVSIESA–AESDFLSYRVEPLKSK-TNFWIGLYR 1412 YP_003965969 619 ———ARTDLELISYKRKDGESVQESSFVKDVKQIMFPNKGSKKKNVNQAKKIAFSDR–SNAFKNIEEVTIGSKV 687 ADU56613 1519 YLSGEHMTSLQNLFKLLNI—EPLSNSDLEFHWLNLATHYPLRMVLRQKIIYSGAVNLEDDRVPTIVKTLQNRLSSTFT 1595 XP_004716076 1413 NVDGMWLWINNNPVSFVNWNTGDPTGERNDCVHLLSASGFWNNIHCSSYKGYICKRPKILEAEPTHTLMTTKAEFRKMGP 1492 YP_003965969 688 KHATFGLGNIINVDTQIISIRFEKIGMKNLAAKICIEKGLLEAVAIADVG—————————— 737 ADU56613 1596 RGAQKLLSEAINKSAFQSSIASGFVGLCRTLGSKCVRGPNRENLYIRSIQSQLLETQGVEAVLGDNGIQIWRVSPEAKDG 1675 XP_004716076 1493 SKASSGVTGVVVTVVLMILVGAG——LTAYFFYKKRRMHPLGEGTFENTLYFNSRSTPGASDTKDLMGNIEQNEHAV 1566 YP_003965969 – ADU56613 1676 D 2220 XP_004716076 1567 I 1567
Selkov data origined here further inquiry. glutamine endpoint orf region above:
The larger emerging premise is as follows:
Rejecting a research avenue of premised causality via in trisomy index case by natural selection, the research potential centers now upon the mannose protein relief. Interestingly, well researched by a Harvard team in 1990. Using the molecular toolbar *Selkov and the reassortment via polar affinity, which within the CNS data has been modified as selective for valene 117 mole weight endpoint pre fold, centric to further model. The homo sapien dynein axoemal heavy polypeptide, an additional contrast available…in regard to spindle residue alignments.
T vaginalis and yersina are two suspect oraganisms, both useful in contrasting data set for study via selkov. Interestingly, the active residues implicated in leishmanasis are also very closely conserved within this initial views of protein reaction chemistries.
An additional outlier arm of observation was the xodies scapularis mechanism as aromatic in evolved conservation, with citris fungi and mycosal interactiolns observed to premise adaptive resistance mechanism toward drug therapy.
Why the research is well served via cartilage assy is observed in AAH 08745 /BAG 53502 with the internal mechanism of gen variant. This is of particular interest when recalling the bat commensual viral load, crossing the species barrier as premised in corona studies. The aleptco species demonstrating a minute but potentially vital clue in the observed viral insult to the regionality of cartilage in homo sapiens as mechanism and pathogenesis.(unpublished). That same slight devation in residue may be causal to the trisomy variant conservation hence produced and conserved in C21 observation.
E. Telafari was my choice to demonstrate the particular intersection to mammal, via
AHK19521 at 188-265 demonstrated via cobalt as a promising selkov relief…to both typical selkov endpoint (204,240)and the newly operant 117. hERE, THE UNDERLYING MOLE WEIGHT AND AFFINITY driving the observational coherence of fold pre blast challenge in observation and subsequent typical blast output…as the end sort….data output regard.
I should pause here, and describe the larger implication.
As I hope the observer can tell, I am interested and motivated in this study. The underlying chemistry of the spindle was perhaps the most difficult, but pictographs were excellent and superb. *EMBO studies. Suggested for backgroud reading but not cited in instance here.
However, application of the fine apparatus in alignment resource, driven by new molecular toolbar resource, demonstrates a narrowing possible regard for mutation adventure.
Revisiting the particular protein residue data generated in the Harvard 1990 paper should be an excellent additive observation as specific to chromosome mutation premised by mechanism…if the mannose avenue is found succinct.
What I do regard as interesting, is that several of the adaptive toolbars and modeling should regard similar chromosomal mechanisms in equally fine relief…..to the regard of SNP…and typical small-large set…specifc to other case presentations at live birth and growth impacted, mechanism impacted at onset *specific to case
The citrus outlier, excellent material to launch a multi drug resistance view. Why? Because it contained Mycobacterium in similarity. I consider here MTB 37Rv.
The largest strength I bring to this work is the recent topic of index case in viral pathogen species, where 17 species are rather fully developed models. This eases the task when rejecting non mammalian terms as regard protein, and remaning centric to the organ studies vital to fully describe the Chromosome as described via OMIM gene map.
Fundamentally, this is a rather interesting topic. While just outside of my usual assay, I rather hope the newly developed tools will meet with continuing use in pathogenesis and homo sapien study via these and premised compound, theraputic design. A natural progression of this work. It does occur to me that within the narrowing focus, certain testing process could begin. Such test would be labeled antibody. Adequate primer design.
Aready demonstrated by protein specific residue and particulars above. Refinement, also, via V Cell model. Available at once.
Research copies of this text are typically saved to a protected data base via google drive.
This eases expense and makes the work aviable to review in every particular.