Question:
- Hide quoted text — Show quoted text – — No, I complained that your thesis relating to tyrosine phosphorylation and skin colouration was "out to lunch" (your words, but not out of context perhaps). I specifically said that it was involved in intracellular signalling, IIRC. J Cell Sci 2001;114(Pt 2):243-244 Related Articles, Books, LinkOut T cell receptor signalling.
Not sure where the relevance of this is in relation to our discussion… <snip That’s not to say tyrosine _metabolism_ isn’t involved in skin colouration, but the two areas (signalling/skin) are as related as bone formation and nerve conduction (both of which use calcium ions). Interesting that you should point out that tyrosine metabolism is as involved with signalling/skin as are bone formation and nerve conduction…
Why? It is the case that the stem cells of the bone marrow give rise to the erythrocytes, etc.
But the stem cells are producing blood cells, not bone cells. The "stem" cells of bone, if you like, are quite seperate in location and lineage from those of the marrow. Marrow just seems a convenient location to produce blood cells. It is the case that nerve cell tissue, particular, glioma tissue, e.g.,
Gliomas are not derived from nerve cells. The glia are the supporting cells that surround CNS neurons. Some provide conduction-improving abilities (oligodendrocytes), some are basically specialised macrophages. I don’t know what they all do…but the glia aren’t nervous tissue. Membranous expression of glucose transporter-1 protein (GLUT-1) in embryonal neoplasms of the central nervous system. Departments of Adult Oncology, Dana Farber Cancer Institute, Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA. The human erythrocyte GLUT-1 is a transmembrane protein which facilitates transport of glucose in the cell in an energy-independent fashion. Neuroectodermal stem cells show strong membrane immunoreactivitry with this marker at early developmental stages in rodents. Membranous expression by undifferentiated neuroectodermal cells gradually decreases while GLUT-1 becomes confined to the endothelial cells, when these acquire blood-brain barrier function.
All this says is it reiterates that embryonal cells (similar to cancerous cells) aren’t as differentiated as normal adult cells. The key fact isn’t that these nerve cells share a erythrocyte marker, but that the marker is what looks like a fairly useful little protein (it controls glucose transport) and that one can use it to distinguish embryonal tumours from tumours of adult tissue that appear in other respects similar. <snip Tyrosine is involved in skin coloration, true, by way of keratinocytes and melanocytes, e.g.:
<snip We’re agreed on this then… <snip You’ve reported exactly what I’ve been trying to tell you all along about tyrosine: now, can you link that specific topic (and not tyrosine in general) to an ability to target one population above another, as you seem to imply was the aim in this paradigm? J Cell Sci 2001;114(Pt 2):243-244 Related Articles, Books, LinkOut T cell receptor signalling.
Whoops – this looks at tyrosine signalling in general. It’s tyrosine phosphorylation, tyrosine residues on _specific_ proteins that are altered by the activity of other _specific_ enzymes in response to cell-cell signals. The use of the amino acid tyrosine as a substrate for melanin is entirely unrelated. Tyrosine phosphorylation induced by C4 peptide constructs from HIV Gp120. Liu M, Zeng J, Robey FA Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Same here. Sorry Bob, but you must take it on board that you really are putting FAR too much store in tyrosine. Nature could have used any amino acid as a signalling mechanism, in fact one of your citations mentions a serine-threonine kinase as well as the tyrosine kinases. It’s just a good one to use, probably because it has a large aromatic ring, as I recall, which is good to use in chemical reactions. Aromatic rings (benzene and the like) are "electron sinks" and can do all sorts of whacky things. Pubmed lists the following amino-acid kinase enzymes under MeSH: Aspartate kinase Arginine kinase Serine-threonine kinase Tyrosine kinase There are over 193,000 references to phosphotransferases, otherwise known as kinases. These are one half of the signalling system using phosphates, the other one being phosphatases. Then you starting looking at the other signalling mechanisms…. Leucine is used in DNA/RNA binding motifs (the so-called leucine-zippers, and zinc fingers). Does that mean that anything involving leucine is linked to DNA/RNA binding? Just because the Sun is yellow, does not mean that everything that is yellow is the Sun, correct? Just because racial characteristics involve tyrosine, does not mean that everything that involves tyrosine is linked to racial characteristics… Cheers Bennett
Response:
–
Nick had complained that my thesis relative to tyrosine phosphorylation and cell-surface targeting was out to lunch. I note this: No, I complained that your thesis relating to tyrosine phosphorylation and skin colouration was "out to lunch" (your words, but not out of context perhaps). I specifically said that it was involved in intracellular signalling, IIRC.
J Cell Sci 2001;114(Pt 2):243-244 Related Articles, Books, LinkOut T cell receptor signalling. Lin J, Weiss A Department of Medicine and The Howard Hughes Medical Institute, University of California, San Francisco, CA 94143-0795, USA. [Record supplied by publisher] Cell Science at a Glance on the Web: electronic copies of the full-size poster insert are available in various formats T cell receptor (TCR) signalling has been an area of intense study for many years. New proteins are being continually discovered each year, making the task of understanding the various pathways evermore challenging. Depicted here are only some of the many TCR-responsive proteins and the mechanisms by which they lead to production of the cytokine interleukin 2 (IL-2). Upon engagement of the TCR by antigen presented on major histocompatibility complex (MHC) molecules, the Src family kinase Lck is activated and proceeds to phosphorylate immunoreceptor tyrosine-based activation motifs (ITAMs) on the &egr;, &dgr;, &ggr; and &zgr; subunits of the TCR. Phosphorylated ITAMs promote the recruitment and subsequent activation of another tyrosine kinase ZAP-70. Two known substrates of ZAP-70 are the adapter molecules LAT and SLP-76. Phosphorylation of tyrosine residues on LAT and SLP-76 results in recruitment of a number of other proteins involved in activation of the Ras pathway, calcium mobilization and cytoskeletal reorganization. One critical protein that is recruited to LAT upon TCR stimulation is phospholipase Cgamma1 (PLCgamma1). Activated PLCgamma1 is responsible for the production of the second messengers diacylglycerol (DAG) and inositol 1,4,5-triphosphate [Ins(1,4,5)P(3)] by cleaving phosphatidylinositol 4,5 bisphosphate [PtdIns(4,5)P(2)] at the plasma membrane. These second messengers are essential for T cell activation. DAG activates a number of proteins, such as the various isoforms of protein kinase C (PKC) and Ras guanyl-nucleotide-releasing protein (RasGRP), whereas Ins(1,4,5)P(3) binds to Ins(1,4,5)P(3 )receptors (Ins(1,4,5)P(3)-Rs) on the surface of the endoplasmic reticulum (ER). Upon Ins(1,4,5)P(3 )receptor binding, Ca(2+) stores in the ER are released into the cytoplasm. This event triggers the opening of Ca(2+)-release-activated Ca(2+) (CRAC) channels at the plasma membrane, allowing influx of extracellular Ca(2+). The increased Ca(2+) levels then activate the protein phosphatase calcineurin by disrupting the inhibitory effects of calmodulin. Calcineurin activation leads to the dephosphorylation of NFAT, allowing it to enter the nucleus, where it cooperates with other transcription factors to bind promoters. Activation of Ras occurs through recruitment of its exchange factors Sos and RasGRP to the membrane. RasGRP contains a C1 domain, which requires binding to DAG for its function. Other proteins, such as the many isoforms of PKC, may also play a role in Ras activation. GTP-bound Ras leads to the activation of a number of serine/threonine kinases and dual-specificity kinases that are responsible for the eventual activation of the mitogen-activated protein (MAP) kinases Erk1/2, JNK and p38. These MAP kinases directly phosphorylate transcription factors involved in the formation of the heterodimeric transcription factor AP-1. Another transcription factor important for the generation of IL-2 is NF-kappaB. Activation of NF-kappaB is dependent on stimulation of the TCR and co-stimulation via CD28. The serine/threonine kinase Akt and the MAP kinase kinase kinases (MAPKKKs) participate in activation of the heterotrimeric IkappaB kinase complex. The IkappaB kinase (IKK) complex regulates NF-kappaB activity by phosphorylating IkappaB, which leads to its ubiquitination. Free from its association with IkappaB, NF-kappaB can move into the nucleus and activate transcription. Many recent studies have focused on functional and physical interactions between the TCR and cytoskeleton. TCR clustering at the site of antigen-presenting cell (APC) contact and re-orientation of the microtubule-organizing center (MTOC) are just some examples. Although proteins such as Vav, Cdc42, Rac and Fyb have been implicated in these events, the exact pathways still remain unclear. The cytoskeleton may also play a role in downregulating IL-2 production by promoting the trafficking of CTLA-4 to the plasma membrane from endosomes. At the plasma membrane, CTLA-4 can then bind its ligand B7-1 or B7-2, causing downregulation by an as-yet-undetermined mechanism. As more research is done, many of the missing pieces are falling into place. Eventually, through the continuing work of many labs, the complex pathways involved in signalling through the TCR should be fully understood. Since T cells play various critical roles in orchestrating the immune responses, this knowledge should lead to an understanding of how breakdowns in immune regulation lead to autoimmune diseases and of how the immune system could be better manipulated to overcome afflictions such as cancer, infection and autoimmune diseases. That’s not to say tyrosine _metabolism_ isn’t involved in skin colouration, but the two areas (signalling/skin) are as related as bone formation and nerve conduction (both of which use calcium ions).
Interesting that you should point out that tyrosine metabolism is as involved with signalling/skin as are bone formation and nerve conduction… It is the case that the stem cells of the bone marrow give rise to the erythrocytes, etc. It is the case that nerve cell tissue, particular, glioma tissue, e.g., Neuropathol Appl Neurobiol 2000 Feb;26(1):91-7 Related Articles, Books, LinkOut Membranous expression of glucose transporter-1 protein (GLUT-1) in embryonal neoplasms of the central nervous system. Loda M, Xu X, Pession A, Vortmeyer A, Giangaspero F Departments of Adult Oncology, Dana Farber Cancer Institute, Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA. The human erythrocyte GLUT-1 is a transmembrane protein which facilitates transport of glucose in the cell in an energy-independent fashion. Neuroectodermal stem cells show strong membrane immunoreactivitry with this marker at early developmental stages in rodents. Membranous expression by undifferentiated neuroectodermal cells gradually decreases while GLUT-1 becomes confined to the endothelial cells, when these acquire blood-brain barrier function. We thus sought to determine whether GLUT-1 expression was limited to embryonal neoplasms of the central nervous system (CNS) which are presumably derived from developmentally arrested neuroectodermal stem cells. Archival material of 40 primary CNS neoplasms were examined for immunoreactivity with anti-GLUT-1. This included both non-embryonal neoplasms (18 astrocytic tumours, one ependymoma and three oligodendroglioma) and embryonal neoplasms (12 cerebellar medulloblastomas, four supratentorial PNETs and two atypical teratoid/rhabdoid tumours (AT/RhT)). In addition, cell lines and nude mice xenografts derived from both undifferentiated and differentiated tumours were assessed for GLUT-1 immunoreactivity by both immunohistochemistry and Western blotting. All embryonal tumours, MBs and PNET xenografts consistently showed GLUT-1 membrane staining. Non-embryonal neoplasms were negative except for vascular staining. Membrane protein fraction of embryonal tumours cell lines immunoreacted by immunoblot with GLUT-1, whereas the glioblastoma cell line was negative. Expression of GLUT-1 supports the stem cell nature of the cells of origin of MBs, supratentorial PNET and AT/RhTs. As a result, GLUT-1 is a useful marker to define the embryonal nature of CNS neoplasms. Tyrosine is involved in skin coloration, true, by way of keratinocytes and melanocytes, e.g.: Cell Mol Biol (Noisy-le-grand) 1999 Nov;45(7):943-9 Related Articles, Books A review of recent advances on the regulation of pigmentation in the human epidermis. Schallreuter KU Clinical and Experimental Dermatology, Department of Biomedical Sciences, It has been recognised that the active transport of L-phenylalanine and its autocrine turnover to L-tyrosine via phenylalanine hydroxylase in the cytosol of epidermal melanocytes provides the majority of the L-tyrosine pool for melanogenesis. In this context, it has been shown that the cofactor 6(R)-L-erythro 5,6,7,8 tetrahydrobiopterin (6BH4) is produced de novo, recycled and regulated in both epidermal melanocytes and keratinocytes to control tyrosine hydroxylase, phenylalanine hydroxylase and tyrosinase activity. Inhibition of the enzymes by excessive 6BH4 levels is reversible with alpha-MSH by specific complex formation between 6BH4 and the hormone. This direct mechanism of alpha-MSH is supported by the presence of the entire POMC processing system in the melanosome indicating a receptor independent control of eumelanogenesis. Finally, the role of tyrosinase, TRP-1 and TRP2 is discussed in association with oxidative stress specifically related to hydrogen peroxide. These recent findings are based on detailed investigations of the depigmentation disorder vitiligo and Hermansky-Pudlak syndrome. Pediatrics 1999 Oct;104(4 Pt 2):1042-5 Related Articles, Books, LinkOut The physiology of pigmented nevi. Kincannon J, Boutzale C Department of Pediatric Dermatology, University of Arkansas for Medical … read more »
Response:
Nick had complained that my thesis relative to tyrosine phosphorylation and cell-surface targeting was out to lunch. I note this:
No, I complained that your thesis relating to tyrosine phosphorylation and skin colouration was "out to lunch" (your words, but not out of context perhaps). I specifically said that it was involved in intracellular signalling, IIRC. That’s not to say tyrosine _metabolism_ isn’t involved in skin colouration, but the two areas (signalling/skin) are as related as bone formation and nerve conduction (both of which use calcium ions). You’ve reported exactly what I’ve been trying to tell you all along about tyrosine: now, can you link that specific topic (and not tyrosine in general) to an ability to target one population above another, as you seem to imply was the aim in this paradigm? Cheers Bennett
Response:
Huh? He points out you are misinterpreting massive amounts of data seeing patterns where in truth none exists. That’s just cutting out the dead wood from the forest so people get a better view of the situation 
That’s probably a good description of it. The point I try to make in my review, is that without the dead wood there’s not much left to convince me. Bob’s book gets polarised reviews I’ve noticed: those that are negative are people who seem to either have a bit of background knowledge, or who aren’t really sure what it adds to the field in terms of finding a solution. That last point is valid, but uncovering any kind of biowarfare research, in particular research which may have gone horribly wrong, could be argued to be in the public interest as an issue quite apart from anything else. Cheers Bennett
Response:
– Hide quoted text — Show quoted text – — — Robert E. Lee, M.S., M.S.W., L.C.S.W. http://www.bhc.edu/eastcampus/leeb/aids/index.html But Bob, any joe blow can become an essentially anonymous reviewer for this site - how do we know that in this case the person has any qualifications to make the aforementioned statement? If they aren’t a molecular biologist or similarly educated, then of what value *IS* this reviewer’s opinion? Garbage in, garbage out. I had asked Nick Bennett to review my book which he did. He placed his review on Amazon.com which is fine by me as he read the book. You’re wandering from the topic at hand – that the review you cite is from an anonymous source that from someone who might not know a well written scientific thesis if it bit them on the ass. Midwest Book Review is a respected reviewer of publications of a scholarly nature. This organization makes its money by delivering useful information. According to this well-respected reviewing agency, "Robert Lee’s AIDS is an important, exhaustively researched, informatively presented, extensive and comprehensive treatise that should be considered a core title for all medical school, public health center, health advocacy organizations, and community library reference collections across the country." This reviewing agency has been in existence for over 20 years. I would suppose that they would not continue to exist were their reviews nonsense. As to Nick’s review, I think it speaks for itself. You have spun a complicated and unlikely scenerio that only can be maintained through faith and ignoring simple probability and all other points of view, as is typical of the genre. I have spun no yarns; the book is no conspiracy theory. It is a report of 1600+ articles from the scientific journals of record documenting the history of the effort to understand, predict, and control immunodeficiency- and immunomodulatory agents including retroviruse in lower species, primates, and humans. I think Nick would be a square-shooter where he to report the forest presented in the book and not a tree.
He did no such thing, he reported the trash science surrounded by misunderstood references. Hope That Helps Anton Wilson did it better 
My book is no conspiracy theory. My book is based on the scientific journals of record.
If you say it often enough maybe even you will begin to believe it’s true eh Bob? — Gary Stein http://www.mischealthaids.org "Usenet is like a herd of performing elephants with diarrhea massive, difficult to redirect, awe-inspiring, entertaining, and a source of mind- boggling amounts of excrement when you least expect it." (Gene Spafford)
Response:
Nick had complained that my thesis relative to tyrosine phosphorylation and cell-surface targeting was out to lunch. I note this: Blood 2001 Feb 1;97(3):608-615 SHP2 and cbl participate in alpha-chemokine receptor CXCR4-mediated signaling pathways. Chernock RD, Cherla RP, Ganju RK Divisions of Experimental Medicine and Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA. Stromal cell-derived factor (SDF)-1alpha and its receptor, CXCR4, play an important role in cell migration, embryonic development, and human immunodeficiency virus infection. However, the cellular signaling pathways that mediate these processes are not fully elucidated. We and others have shown that the binding of SDF-1alpha to CXCR4 activates phosphatidylinositol-3 kinase (PI-3 kinase), p44/42 mitogen-associated protein kinase, and the transcription factor nuclear factor-kappaB, and it also enhances the tyrosine phosphorylation and association of proteins involved in the formation of focal adhesions. In this study, we examined the role of phosphatases in CXCR4-mediated signaling pathways. We observed significant inhibition of SDF-1alpha-induced migration by phosphatase inhibitors in CXCR4-transfected pre-B lymphoma L1.2 cells, Jurkat T cells, and peripheral blood lymphocytes. Further studies revealed that SDF-1alpha stimulation induced robust tyrosine phosphorylation in the SH2-containing phosphatase SHP2. SHP2 associated with the CXCR4 receptor and the signaling molecules SHIP, cbl, and fyn. Overexpression of wild-type SHP2 increased SDF-1alpha-induced chemotaxis. Enhanced activation of fyn and lyn kinases and the tyrosine phosphorylation of cbl were also observed. In addition, SDF-1alpha stimulation enhanced the association of cbl with PI-3 kinase, Crk-L, and 14-3-3beta proteins. Our results suggest that CXCR4-mediated signaling is regulated by SHP2 and cbl, which collectively participate in the formation of a multimeric signaling complex. (Blood. 2001;97:608-615) J Biol Chem 2000 Jun 9;275(23):17263- Beta-chemokine receptor CCR5 signals through SHP1, SHP2, and Syk. Ganju RK, Brubaker SA, Chernock RD, Avraham S, Groopman JE Division of Experimental Medicine, Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts The beta-chemokine receptor CCR5 has been shown to modulate cell migration, proliferation, and immune functions and to serve as a co-receptor for the human immunodeficiency virus. We and others have shown that CCR5 activates related adhesion focal tyrosine kinase (RAFTK)/Pyk2/CAK-beta. In this study, we further characterize the signaling molecules activated by CCR5 upon binding to its cognate ligand, macrophage inflammatory protein-1beta (MIP1beta). We observed enhanced tyrosine phosphorylation of the phosphatases SHP1 and SHP2 upon MIP1beta stimulation of CCR5 L1.2 transfectants and T-cells derived from peripheral blood mononuclear cells. Furthermore, we observed that SHP1 associated with RAFTK. However, using a dominant-negative phosphatase-binding mutant of RAFTK (RAFTK(m906)), we found that RAFTK does not mediate SHP1 or SHP2 phosphorylation. SHP1 and SHP2 also associated with the adaptor protein Grb2 and the Src-related kinase Syk. Pretreatment of CCR5 L1.2 transfectants or T-cells with the phosphatase inhibitor orthovanadate markedly abolished MIP1beta-induced chemotaxis. Syk was also activated upon MIP1beta stimulation of CCR5 L1.2 transfectants or T-cells and associated with RAFTK. Overexpression of a dominant-negative Src-binding mutant of RAFTK (RAFTK(m402)) significantly attenuated Syk activation, whereas overexpression of wild-type RAFTK enhanced Syk activity, indicating that RAFTK acts upstream of CCR5-mediated Syk activation. Taken together, these results suggest that MIP1beta stimulation mediated by CCR5 induces the formation of a signaling complex consisting of RAFTK, Syk, SHP1, and Grb2. Cell 1998 Oct 16;95(2):163-75 Nef harbors a major determinant of pathogenicity for an AIDS-like disease induced by HIV-1 in transgenic mice. Hanna Z, Kay DG, Rebai N, Guimond A, Jothy S, Jolicoeur P Clinical Research Institute of Montreal, Department of Medicine, Universite de Montreal, Quebec, Canada. Transgenic (Tg) mice expressing the complete coding sequences of HIV-1 in CD4+ T cells and in cells of the macrophage/dendritic lineages develop severe AIDS-like pathologies: failure to thrive/weight loss, diarrhea, wasting, premature death, thymus atrophy, loss of CD4+ T cells, interstitial pneumonitis, and tubulo-interstitial nephritis. The generation of Tg mice expressing selected HIV-1 gene(s) revealed that nef harbors a major disease determinant. The latency and progression (fast/slow) of the disease were strongly correlated with the levels of Tg expression. Nef-expressing Tg thymocytes were activated and alpha-CD3 hyperresponsive with respect to tyrosine phosphorylation of several substrates, including LAT and MAPK. The similarity of this mouse model to human AIDS, particularly pediatric AIDS, suggests that Nef may play a critical role in human AIDS, independently of its role in virus replication.
Response:
–
– Hide quoted text — Show quoted text – — Robert E. Lee, M.S., M.S.W., L.C.S.W. http://www.bhc.edu/eastcampus/leeb/aids/index.html But Bob, any joe blow can become an essentially anonymous reviewer for this site - how do we know that in this case the person has any qualifications to make the aforementioned statement? If they aren’t a molecular biologist or similarly educated, then of what value *IS* this reviewer’s opinion? Garbage in, garbage out. I had asked Nick Bennett to review my book which he did. He placed his review on Amazon.com which is fine by me as he read the book. You’re wandering from the topic at hand – that the review you cite is from an anonymous source that from someone who might not know a well written scientific thesis if it bit them on the ass.
Midwest Book Review is a respected reviewer of publications of a scholarly nature. This organization makes its money by delivering useful information. According to this well-respected reviewing agency, "Robert Lee’s AIDS is an important, exhaustively researched, informatively presented, extensive and comprehensive treatise that should be considered a core title for all medical school, public health center, health advocacy organizations, and community library reference collections across the country." This reviewing agency has been in existence for over 20 years. I would suppose that they would not continue to exist were their reviews nonsense. As to Nick’s review, I think it speaks for itself. You have spun a complicated and unlikely scenerio that only can be maintained through faith and ignoring simple probability and all other points of view, as is typical of the genre.
I have spun no yarns; the book is no conspiracy theory. It is a report of 1600+ articles from the scientific journals of record documenting the history of the effort to understand, predict, and control immunodeficiency- and immunomodulatory agents including retroviruse in lower species, primates, and humans. I think Nick would be a square-shooter where he to report the forest presented in the book and not a tree. Anton Wilson did it better
My book is no conspiracy theory. My book is based on the scientific journals of record. — Robert E. Lee, M.S., M.S.W., L.C.S.W. http://www.bhc.edu/eastcampus/leeb/aids/index.html
Response:
From Nick’s review on Amazon.com: "The errors of fact, theory and understanding are so abundant, numbering two or three on nearly every one of the 502 pages of the book, that it would be impossible for me to list and explain them all without writing a tome of similar size." This would be at least 1,000 to 1,500 errors as per Nick’s own words. This is not a fair statement. I have asked for 20 and he has given me about 10 with some of these being interpretational ambiguities.
Okay, but if you’d say which of those I posted to MHA were interpretational, and which were valid errors, that’d help. Nick says in the review: "He makes the critical error of looking for evidence to support his apparently pre-supposed idea that there was a scientific "paradigm" (read "conspiracy") to develop and use a biowarfare agent in the unlikely form of a chronic retrovirus infection." The book contains 1600 references from the scientific journals of record. I did not look for evidence to support anything; I reported who did what, when, in what animal, with what virus. The paradigm reveals itself in this analysis.
No, it does not. You put forward one _possible_ interpretation of this work, but the work itself does not make this conclusion the most likely one, not by a long shot. In addition, you word your writing such that it appears (hence the words "APPARENTLY pre-supposed") that you have come to your conclusion prior to presenting the evidence. Nick says, "My girlfriend laughed so hard at this book she cried." I hardly think this is a fair review; there is no citation of page/issue… it is the objective of the review to make the book look like it is some sort of idiot’s work.
The specific section where she laughed was the phrase "lactase intolerance", when you probably meant "lactose intolerance", and tried to implicate work on said subject to targetting non-caucasian populations. Nick says, "The sad thing is that had he had input from a research assistant of any half-decent laboratory, most of his errors would have been spotted. This would have meant that most, if not all, of his case would have been rendered redundant: this book need never have been written." IF the book is so error-laden with mistakes that negate the thesis of the book that could have been found by any research assistant of any half-decent laboratory, then you would think it would be simple matter for a Cambridge, UK, molecular biologist MD/PhD teacher/student to articulate in 3 paragraphs the absolute core issues that invalidate the book. Nick has not done this.
But I have, specifically: There are multiple errors: I couldn’t not list them all for what was obviously a review designed for the masses on Amazon, with a word limit. These errors either detract directly from the arguments presented, or bring doubt onto the work in general. The argument is not properly formulated: i.e. it does not make logical sense, and seems to be based upon speculation and then evidence, as opposed to the other way around. That may not be the case, but THAT IS HOW IT APPEARED. This isn’t the correct way to convincingly show anything in science, and I approached this book in the same way I approach a journal article for critical review, which is done about twice a week to a greater or lesser degree. To someone in the field it makes no sense: this is perhaps the biggest problem with the book. It was written by someone in a different field, someone with no formal training in that field, and (perhaps through no fault of the author) without the assistance of anyone in that field. In the same way as I would never tell a ballerina how to dance, why should a non-scientist tell scientists how to interpret the literature? He is dancing around the issues and is not addressing the larger fundamental issue: the book details an 80 year scientific paradigm devoted to the understanding, prediction, and control of immunodeficiency and immuno-modulatory agents and their association with various animal retroviruses and human variables including ethnic differences in virus docking at the cell surface of lymphocytes — HLA. It is my opinion that Nick has focused on a tree and has lost sight of the forest.
Bob, I don’t deny the work focusses on that which you say: but I can’t see how you can convincingly show that such work was done for any purpose other than the advancement of knowledge. To many people (myself included), knowledge is not a means to an end, it is an end in itself. Cheers Bennett
Response:
–
– Hide quoted text — Show quoted text – He has told you repeatedly that he is very busy and will get back to your questions when he has time, after all it is not his job to teach you the science you are so obviously lacking. No, but I did offer 
) There are two things that are stopping me from a play-by-play analysis of Bob’s book: the time it would take to go through the book page by page, and to type in my comments: I’d end up with a file as large as Bob’s book, as far as I can tell. I’m also not keen on appearing to attack Bob, who gave me a _free_ copy in good faith, not expecting me to come down on the side I did. On the other hand, I do think my conclusions are fair, which doesn’t mean I betrayed any trust he had in _that_. Bennett
From Nick’s review on Amazon.com: "The errors of fact, theory and understanding are so abundant, numbering two or three on nearly every one of the 502 pages of the book, that it would be impossible for me to list and explain them all without writing a tome of similar size." This would be at least 1,000 to 1,500 errors as per Nick’s own words. This is not a fair statement. I have asked for 20 and he has given me about 10 with some of these being interpretational ambiguities. Nick says in the review: "He makes the critical error of looking for evidence to support his apparently pre-supposed idea that there was a scientific "paradigm" (read "conspiracy") to develop and use a biowarfare agent in the unlikely form of a chronic retrovirus infection." The book contains 1600 references from the scientific journals of record. I did not look for evidence to support anything; I reported who did what, when, in what animal, with what virus. The paradigm reveals itself in this analysis. Nick says, "My girlfriend laughed so hard at this book she cried." I hardly think this is a fair review; there is no citation of page/issue… it is the objective of the review to make the book look like it is some sort of idiot’s work. Nick says, "The sad thing is that had he had input from a research assistant of any half-decent laboratory, most of his errors would have been spotted. This would have meant that most, if not all, of his case would have been rendered redundant: this book need never have been written." IF the book is so error-laden with mistakes that negate the thesis of the book that could have been found by any research assistant of any half-decent laboratory, then you would think it would be simple matter for a Cambridge, UK, molecular biologist MD/PhD teacher/student to articulate in 3 paragraphs the absolute core issues that invalidate the book. Nick has not done this. He is dancing around the issues and is not addressing the larger fundamental issue: the book details an 80 year scientific paradigm devoted to the understanding, prediction, and control of immunodeficiency and immuno-modulatory agents and their association with various animal retroviruses and human variables including ethnic differences in virus docking at the cell surface of lymphocytes — HLA. It is my opinion that Nick has focused on a tree and has lost sight of the forest.
Response:
How many copies have you sold so far Bob? — Gary The book is in its second printing. The book is not a New York Times Best-seller, for sure, and was not intended to be thus. It is a science book.
That does not answer the question a simple number would suffice. — Gary Stein http://www.mischealthaids.org "Usenet is like a herd of performing elephants with diarrhea massive, difficult to redirect, awe-inspiring, entertaining, and a source of mind- boggling amounts of excrement when you least expect it." (Gene Spafford) – Hide quoted text — Show quoted text – The book is for sale on all the various electronic book sales chains and is in the holdings of various libraries around the nation. I would have to talk to my publisher concerning exact numbers. http://www.bestwebbuys.com/books/compare?isbn=1929882033
Response:
He has told you repeatedly that he is very busy and will get back to your questions when he has time, after all it is not his job to teach you the science you are so obviously lacking.
No, but I did offer ) There are two things that are stopping me from a play-by-play analysis of Bob’s book: the time it would take to go through the book page by page, and to type in my comments: I’d end up with a file as large as Bob’s book, as far as I can tell. I’m also not keen on appearing to attack Bob, who gave me a _free_ copy in good faith, not expecting me to come down on the side I did. On the other hand, I do think my conclusions are fair, which doesn’t mean I betrayed any trust he had in _that_. Bennett
Response:
I had asked Nick Bennett to review my book which he did. He placed his review on Amazon.com which is fine by me as he read the book. He states in his review there are at least 1,000 errors in the book.
I actually said there were a few on most pages, which could add up to about 1000 in total. I haven’t counted them all: nor I suppose does that include the reference pages. I have asked him to tell me 20 and he has told me about 10 at the most and some of these are matters of interpretation and are not errors.
Did you post a reply to the message I sent to MHA? I’ve not seen anything (not really been looking much of late…) If you consider some of them matters of interpretation then say which specifically and I’ll let you know if that’s the case, of if I’m relying on a source other than my opinion. The book sets out in very clearly articulated means the entire scientific paradigm of the pursuit of immunodeficiency-causing and immuno-modulatory agents over 80 years. Nick Bennet does not once address this other than to say there is a conspiracy or something similar to that… which is blatant nonsense.
Bob, the possibility that such a pursuit would even occur is unlikely. The concept is unfeasible in terms of a biowarfare agent, and unrealistic in terms of the molecular biology of the day. The idea that this research would be publically acknowledged in the peer-reviewed literature, when one would expect it to be kept under tight military control and with limited dissemination, seems extremely counter-intuitive. The evidence you present should, IMHO, be interpreted only to mean that the scientists were researching agents X Y and Z, and not that they were aiming to produce agents A B or C. As I said before: scientists have been researching the fruit fly in terms of genetic manipulation for decades, but does this mean that the results are to be used in a genetically-specific biowarfare weapon? Are mosquitoes actually military sampling devices to gather DNA from the population? The molecular biologists that I have dealt with on here are not really interested in knowing this big picture, in my opinion.
Bob – Mike and I took the time to read your stuff and comment on it. We would be interested if there was some substance to the claims. _IF_ such a program was in existence then your book does not prove it to me in any way. You presented very little data that solidly supported your case, which was composed of governmental memo’s and other official documents. I found these far more interesting and relevant than reports on LDV or blood typing. Cheers Bennett
Response:
How many copies have you sold so far Bob? — Gary
The book is in its second printing. The book is not a New York Times Best-seller, for sure, and was not intended to be thus. It is a science book. The book is for sale on all the various electronic book sales chains and is in the holdings of various libraries around the nation. I would have to talk to my publisher concerning exact numbers. http://www.bestwebbuys.com/books/compare?isbn=1929882033
Response:
Go here to find out information about the book’s availability: http://isbn.nu/1929882033/price http://www.addall.com/New/compare.cgi?dispCurr=USD&id=86493&isbn=1929… location=10000&thetime=20010218192202&state=AK
Response:
– Hide quoted text — Show quoted text – — Robert E. Lee, M.S., M.S.W., L.C.S.W. http://www.bhc.edu/eastcampus/leeb/aids/index.html But Bob, any joe blow can become an essentially anonymous reviewer for this site - how do we know that in this case the person has any qualifications to make the aforementioned statement? If they aren’t a molecular biologist or similarly educated, then of what value *IS* this reviewer’s opinion? Garbage in, garbage out. I had asked Nick Bennett to review my book which he did. He placed his review on Amazon.com which is fine by me as he read the book. He states in his review there are at least 1,000 errors in the book. I have asked him to tell me 20 and he has told me about 10 at the most and some of these are matters of interpretation and are not errors. I asked him about this and he says that the "2 or 3 errors on nearly every page of the book" are, perhaps, repetitions of a single error. I contest this. As I have come to consider his review a bit more, I am totally dissatisfied with it. It is not an accurate portrayal of the book, in my opinion.
Of course it’s not you have to date refused any critcism no matter how mild, if the review is not glowing you automatcally call it a hatchet job. As to your "issues of interpretation" Nick covered that with you quite clearly and in most other readers opinion you came out on the wrong side of the disscussion. He is entitled to his opinion but he has demonstrated in his review and subsequent follow up of the alledged errors that he has had no real intention of addressing the evidence.
He has told you repeatedly that he is very busy and will get back to your questions when he has time, after all it is not his job to teach you the science you are so obviously lacking. — Gary Stein http://www.mischealthaids.org "Usenet is like a herd of performing elephants with diarrhea massive, difficult to redirect, awe-inspiring, entertaining, and a source of mind- boggling amounts of excrement when you least expect it." (Gene Spafford) – Hide quoted text — Show quoted text – The book sets out in very clearly articulated means the entire scientific paradigm of the pursuit of immunodeficiency-causing and immuno-modulatory agents over 80 years. Nick Bennet does not once address this other than to say there is a conspiracy or something similar to that… which is blatant nonsense. The molecular biologists that I have dealt with on here are not really interested in knowing this big picture, in my opinion. Therefore, we have a variance: a couple of molecular biologists on here would like to trash the book; I have had several medical doctors rave about the book; I have reviews by respected reviewing agencies saying the book is "core reading" or "a must have book" and I have been on the radio now at least a half-dozen times regarding the topic. Just as AIDS, itself, has be politicized, so, too, has this book fallen into the same status. I am noting that since my book has been published in which I articulate the historic efforts to design bioweaponry with the objective of selectively targeting particular ethnic groups that there has been a media-storm concerning the human genome project, DNA, viruses, and other related topics with very similar concerns. It is amusing to me to note that the discussion of the concerns with these various areas is exactly what I have articulated in my book. Moreover, and wisely so, the European community has finally realized what killer is on the loose in Mad-Cow diseases. This book is making its projected impact and it will continue to gain momentum as time goes on. I have been cited by others already and will be so in the future. GIGO, indeed. When the truth about the SVCP comes out in a big way as a result of all the various plagues related to it being finally realized by the general public, there are going to be a few books that have led the way in this. My book, along with those of Dr. Len Horowitz, Dr. Alan Cantwell, Dr. Willliam Douglas, and Dr. Robert Strecker, is one of those books. More will be written… Time is on our side, yes it is.
Response:
— Robert E. Lee, M.S., M.S.W., L.C.S.W. http://www.bhc.edu/eastcampus/leeb/aids/index.html But Bob, any joe blow can become an essentially anonymous reviewer for this site - how do we know that in this case the person has any qualifications to make the aforementioned statement? If they aren’t a molecular biologist or similarly educated, then of what value *IS* this reviewer’s opinion? Garbage in, garbage out.
I had asked Nick Bennett to review my book which he did. He placed his review on Amazon.com which is fine by me as he read the book. He states in his review there are at least 1,000 errors in the book. I have asked him to tell me 20 and he has told me about 10 at the most and some of these are matters of interpretation and are not errors. I asked him about this and he says that the "2 or 3 errors on nearly every page of the book" are, perhaps, repetitions of a single error. I contest this. As I have come to consider his review a bit more, I am totally dissatisfied with it. It is not an accurate portrayal of the book, in my opinion. He is entitled to his opinion but he has demonstrated in his review and subsequent follow up of the alledged errors that he has had no real intention of addressing the evidence. The book sets out in very clearly articulated means the entire scientific paradigm of the pursuit of immunodeficiency-causing and immuno-modulatory agents over 80 years. Nick Bennet does not once address this other than to say there is a conspiracy or something similar to that… which is blatant nonsense. The molecular biologists that I have dealt with on here are not really interested in knowing this big picture, in my opinion. Therefore, we have a variance: a couple of molecular biologists on here would like to trash the book; I have had several medical doctors rave about the book; I have reviews by respected reviewing agencies saying the book is "core reading" or "a must have book" and I have been on the radio now at least a half-dozen times regarding the topic. Just as AIDS, itself, has be politicized, so, too, has this book fallen into the same status. I am noting that since my book has been published in which I articulate the historic efforts to design bioweaponry with the objective of selectively targeting particular ethnic groups that there has been a media-storm concerning the human genome project, DNA, viruses, and other related topics with very similar concerns. It is amusing to me to note that the discussion of the concerns with these various areas is exactly what I have articulated in my book. Moreover, and wisely so, the European community has finally realized what killer is on the loose in Mad-Cow diseases. This book is making its projected impact and it will continue to gain momentum as time goes on. I have been cited by others already and will be so in the future. GIGO, indeed. When the truth about the SVCP comes out in a big way as a result of all the various plagues related to it being finally realized by the general public, there are going to be a few books that have led the way in this. My book, along with those of Dr. Len Horowitz, Dr. Alan Cantwell, Dr. Willliam Douglas, and Dr. Robert Strecker, is one of those books. More will be written… Time is on our side, yes it is.
Response:
My book "AIDS: An Explosion of the Biological Time-bomb?" has been reviewed by Midwest Book Review. This is a well known and highly respected reviewing firm in the publishing business. The review states: "Robert Lee’s AIDS is an important, exhaustively researched, informatively presented, extensive and comprehensive treatise that should be considered a core title for all medical school, public health center, health advocacy organizations, and community library reference collections across the country." See here: http://www.execpc.com/~mbr/bookwatch/ibw/ This is a good book despite the hatchet jobs from the molecular biology people. — Robert E. Lee, M.S., M.S.W., L.C.S.W. http://www.bhc.edu/eastcampus/leeb/aids/index.html
Response:
– Hide quoted text — Show quoted text – My book "AIDS: An Explosion of the Biological Time-bomb?" has been reviewed by Midwest Book Review. This is a well known and highly respected reviewing firm in the publishing business. The review states: "Robert Lee’s AIDS is an important, exhaustively researched, informatively presented, extensive and comprehensive treatise that should be considered a core title for all medical school, public health center, health advocacy organizations, and community library reference collections across the country." See here: http://www.execpc.com/~mbr/bookwatch/ibw/ This is a good book despite the hatchet jobs from the molecular biology people.
How many copies have you sold so far Bob? — Gary Stein http://www.mischealthaids.org "Usenet is like a herd of performing elephants with diarrhea massive, difficult to redirect, awe-inspiring, entertaining, and a source of mind- boggling amounts of excrement when you least expect it." (Gene Spafford) – Hide quoted text — Show quoted text – — Robert E. Lee, M.S., M.S.W., L.C.S.W. http://www.bhc.edu/eastcampus/leeb/aids/index.html
Response:
Posted in Interstitial Nephritis | 
No Comments » | 