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A hypothesis that proposes that defects in PHD2 and PHD3 function may be causal of the symptoms of schizopnrenia. By John Neville
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A defect in the coactivation of HIF1 by PKM2 and PHD3 has been implicated in a familial disorder which can cause autoinflammatory symptoms, connective tissue symptoms and psychosis. It has also been... More > pointed out that a majority of predicted target genes of HIF1 are associated with schizopnrenia, or have altered function or expression in schizopnrenia. PHD2 and PHD3 both regulate HIF1a. Here it is noted that PHD2 (EGLN1) is located at 1q42.2, very close to the location of DISC1 and DISC2, whilst PHD3 (EGLN3) is located at 14q13.1, very close to the location of NPAS3. The disruption of DISC1 and DISC2 genes by a translocation co-segregating with familial schizopnrenia is well known. A mutation in NPAS3 also segregates with schizophrenia in a small family. This raises the interesting possibility that defective PHD2 and PHD3 function could be causal of the symptoms of schizopnrenia.< Less
Defective binding of a PPARG and STAT1 complex to the CD36 promotor is implicated in a familial disorder which can cause autoinflammatory symptoms, connective tissue symptoms and psychosis. By John Neville
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The binding of a PPARG and STAT1 complex to the STAT binding site at -107 nucleotides in the CD36 promotor is identified as an interaction which very directly links to the main genes and metabolic... More > pathways previously implicated in a familial disorder, suggesting that defective binding of this PPARG and STAT1 complex to the CD36 promotor should play a central role in the aetiology of the familial disorder. The same interaction may be of significance in autoinflammatory disorders more generally.< Less
A hypothesis that proposes that immune response reactions may cause the rapid acquirement of pathologically significant SNPs, allele combinations and/or runs of homozygosity in rheumatoid arthritis and Parkinson’s disease. By John Neville
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It was previously hypothesized that many SNPs that are associated with schizophrenia could be acquired rapidly in one generation as part of an immune response reaction. It is now hypothesized that... More > the same or a similar process could be responsible for some cases of rheumatoid arthritis (RA) and Parkinson’s disease.< Less
Analysing and attempting to connect the genetic and metabolic derangements underpinning a disorder which is linked to schizophrenia in Irish high density schizophrenia families (see preview to check for availability of free access). By John Neville
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A familial disorder that causes psychosis is described. Associated with the disorder are distinct patterns of physical symptoms and conditions that may be used to assist diagnosis. The proband... More > carries genetic markers that link the disorder to schizophrenia in Irish high density schizophrenia families. The genetic and metabolic derangements underpinning the disorder are analysed and potentially linked. Evidence is considered which supports a working hypothesis in which haplotype SNPs located at IL3 and/or ACSL6 at 5q31.1 result in or from the failure or partial failure of one or more ERE to activate a pathway leading from P5CS to proline.< Less
The Big Bang and Steady State Universe – a unifying theory. By John Neville
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It is hypothesized that all matter in the universe is sucked back at varying points in time and space to the moment and location of the Big Bang. Thus the matter/energy given off by the Big Bang is... More > repeatedly used as fuel for the Big Bang, which repeats presumably endlessly at the same location and time. Thus the universe has the Big Bang at the start but is also in a constant state. The force that sucks matter/energy back to the Big Bang explains gravity. The matter/energy of the universe is thus both finite and infinite in its being. Dark energy is the force that in the future sucks currently existing matter back to the place and time of the Big Bang. As more time passes the amount of dark matter should increase, and the amount of dark energy will also alter. At the end of time, the amount of dark matter should be 100% of the matter in the universe and dark energy will cease to exist.< Less
CCNB1, CCNB2, CCNA1, CCNA2, SYT1, SYT2, CKS2, CKS1B, CCNB3, SKP1, CDK1, RPS23, RPS27A, ZFAND4, RPS27, RPS27l, BUB1, BUB1B could play significant roles in the aetiology of schizophrenia by acting as points of contact between ALDH18A1 and SEC23IP (COP2). By John Neville
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Fourteen genes and their paralogues (CCNB1, CCNB2, CCNA1, CCNA2, SYT1, SYT2, CKS2, CKS1b, CCNB3, RPS23, RPS27A, ZFAND4, RPS27, RPS27l, BUB1, BUB1B, SKP1, CDK1), which putatively act as points of... More > contact between ALDH18A1 and COP2 associated genes, particularly SEC23IP and CSNK1D, are identified which could play significant roles in the aetiology of schizophrenia. Many of these genes are found at the same genetic locations as deletion/duplication disorders and/or CNVs that have been reported on as being associated with schizophrenia. A partial failure of SEC23IP binding is identified as a possible cause of symptoms of 22q Parkinson's disease. Proline residues are identified as possible treatment targets in 22q Parkinson's disease.< Less
Paragangliomas and schizophrenia linked to EGLN1, EGLN2, EGLN3 and DISC1 function. By John Neville
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Previously evidence was considered which raised the interesting possibility that defective EGLN1 and EGLN3 function could be causal of the symptoms of schizopnrenia. Here it is pointed out that... More > EGLN1, EGLN2, EGLN3, DISC1 are either functional for or strongly associated with paragangliomas, which are well known to cause anxiety and panic, but which can also cause psychosis which can remit with removal of the tumour. This raises various questions of importance which may well lead to the identifying of biomarkers for one of the causes of psychosis and novel treatments.< Less
The interaction of HIF1a, ammonia and NMDAR subunits is identified as a location of particular interest in schizophrenia, and MIR190a is identified as a candidate location for a familial disorder which substantially increases the risk of psychosis. By John Neville
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The interaction of HIF1a, ammonia and NMDAR subunits is identified as a location of particular interest in schizophrenia, and MIR190a is identified as a candidate location for a familial disorder... More > which substantially increases the risk of psychosis.< Less
A defect in the coactivation of HIF1 by PKM2 and PHD3 is implicated in a familial disorder which can cause autoinflammatory symptoms, connective tissue symptoms and psychosis. By John Neville
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A defect in the coactivation of HIF1 by PKM2 and PHD3 (interaction 1) is implicated in a familial disorder which can cause autoinflammatory symptoms, connective tissue symptoms and psychosis. It is... More > suggested that interaction 1 may act in concert with the binding of a STAT1/PPARG complex to the CD36 promotor (interaction 2) to regulate the flux of pyrroline-5-carboxylic acid, whether to proline synthesis or to the urea cycle. It is proposed that these two interactions may provide for viable treatment targets in schizophrenia where hyperprolinemia is present.< Less
A hypothesis that proposes that in ALDH18A1 spastic paraplegia, the failure to produce specific proline residues required for the binding of SEC23IP as part of the COP2 transport process could be causative of symptoms and may be a viable treatment target By John Neville
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It is hypothesized that a failure or partial failure of ALDH18A1/PYCR1 to produce specific proline residues could be causative of symptoms in ALDH18A1 spastic paraplegia and also of symptoms in... More > ALDH18A1/PYCR1 cutis laxa. If so, any such missing proline residues may be viable treatment targets. In the case of ALDH18A1 spastic paraplegia, these proline residues would be required for the binding of SEC23IP/PI3P, whilst in the case of ALDH18A1/PYCR1 cutis laxa, the proline residues would be required for the formation of elastin. Contains approximately forty blank pages.< Less

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LOOKING FOR A MIRACLE...LOOK WITHIN YOUR LIFE LOOKING FOR A... By May Lewis
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