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2012 - 1202(1) - 1204(2) - 1205(1) - 1210(1) - 1212(1)
2013 - 1302(3) - 1303(1) - 1304(3)
Any replacements are listed further down
[22] viXra:1304.0162 [pdf] submitted on 2013-04-29 17:19:16
Authors: Fabrice Pautot
Comments: 24 Pages.
In vivo tracer kinetics, as probed by current tomographic techniques, is revisited from the point of view of fluid kinematics. Proofs of the standard intravascular advective perfusion model from first premises reveal underlying assumptions and demonstrate that all single input models apply at best to undefined tube-like systems, not to the ones defined by tomography, \textit{i.e.} the voxels. In particular, they do not and cannot account for the circulation across them. More generally, it is simply not possible to define a single non-zero steady volumetric flow rate per voxel. Restarting from the fact that kinematics requires the definition of six volumetric flow rates per voxel, one for each face, minimalist, 4D spatiotemporal analytic models of the advective transport of intravascular tracers in the whole organ of interest are obtained. Their many parameters, plasmatic volumetric flow rates and volumes, can be readily estimated at least in some specific cases. Estimates should be quasi-absolute in homogeneous tissue regions, regardless of the tomographic technique. Potential applications such as dynamic angio-tractography are presented. By contrast, the transport of mixed intra/extravascular tracers cannot be described by conservation of the mass alone and requires further investigation. Should this theory eventually supersede the current one(s), it shall have a deep impact on our understanding of the circulatory system, hemodynamics, perfusion, permeation and metabolic processes and on the clinical applications of tracer tracking tomography to numerous pathologies.
Category: Quantitative Biology
[21] viXra:1304.0056 [pdf] submitted on 2013-04-11 17:09:55
Authors: Li Xia
Comments: 30 Pages.
Using the computational approach, we studied the oligonucleotides repeats in current available bacterial whole genomes. Though, repeats only count for a small portion in bacterial genomes, they still prevail. Our study shows, some of these oligonucleotides
have a large copy number in genomes while maintain its taxon specificity. Generally, a length larger than 12 is enough to make a oligonucleotides repeats genus specific. Longer oligonucleotides will become more specific and be the species or strain
marker sequences. We show here some examples in archaea and bacteria with different specific taxon levels. As we have a large volume of computational results, we make it available online by our TSOR server.It deals with user’s query and in this thesis we
give examples on how to use this server. Moreover as these TSOR sequences are both specific and highly repeated, they would become possible nice candidate for biased microbial community genomes amplification
Category: Quantitative Biology
[20] viXra:1304.0028 [pdf] submitted on 2013-04-05 07:25:31
Authors: Stan Bumble
Comments: 36 Pages.
The following is a power point presentation
on Systems Biology including aspects of Self-Organization and Emergence.
Category: Quantitative Biology
[19] viXra:1303.0027 [pdf] submitted on 2013-03-05 11:50:58
Authors: Andrew Nassif
Comments: 18 Pages.
Andrew Nassif's guide on the world of microbes and the rise of its cellular growth as a colony.
Category: Quantitative Biology
[18] viXra:1302.0092 [pdf] submitted on 2013-02-13 17:20:12
Authors: Alan Williams
Comments: 5 Pages.
Ventricular Septal Defects (VSD) and Pulmonary Vein Stenosis (PVS) are both normally non- life- threatening problems for survivors of early
childhood. However, it can be a large hindrance to many patients who want a
normal life. With this proposed solution, patients should be able to achieve
a life mostly free of problems. Hopefully, only regular check-ups will be
required after the initial treatment.
Category: Quantitative Biology
[17] viXra:1302.0078 [pdf] submitted on 2013-02-12 22:32:18
Authors: Mark R. Brenneman
Comments: 1 Page. emissrto@yahoo.com
Spectrin isoforms are found in erythroid and nonerythroid cells. Spectrin is a component (known as the postsynaptic density (PSD)) for the maintenance of cell cytoskeleton shape the main fibrous component of which is spectrin of the erythrocyte membrane controlling Smad3/4 subcellular localization in TGFβ/Smad signalling resulting in nuclear translocation of activated Smad4. beta subunit-fodrin, spectrin-like protein, is a nonerythroid spectrin analogue alpha Spna-1 related to human erythrocytic 1 (hSPTBN1) Nonerythroid brain spectrin (Spnb-2 Beta-II spectrin). Three isoforms of brain spectrin contains three structural domains. A nonerythroid 9 Kb mRNA which encodes neuronal beta SpIIa occurs also in neonatal cardiomyocytes with ankyrin-B and ELF (Spnb-2), a new isoform of beta-G-spectrin. Spnb2 js found to cross-react with human erythrocyte beta subunit spectrin-ankyrin scaffold in restoring similarity of structure to lateral membrane biogenesis, cross-linking protein alpha-chain, and the Actin binding N-terminal domain of beta-chain, a form of exon/intron usage of two antiparallel dimers usage Complementary DNA synthesized from a messenger mRNA a stem cell adaptor protein is found in two to four cells per 30,000-50,000 cells.
Category: Quantitative Biology
[16] viXra:1302.0027 [pdf] submitted on 2013-02-04 16:39:12
Authors: Nathan O. Schmidt
Comments: 130 pages and 18 figures
A regular expression and region-specific filtering system for biological records at the National Center for Biotechnology database is integrated into an object-oriented sequence counting application, and a statistical software suite is designed and deployed to interpret the resulting k-mer frequencies---with a priority focus on nullomers. The proteome k-mer frequency spectra of ten model organisms and the genome k-mer frequency spectra of two bacteria and virus strains for the coding and non-coding regions are comparatively scrutinized. We observe that the naturally-evolved (NCBI/organism) and the artificially-biased (randomly-generated) sequences exhibit a clear deviation from the artificially-unbiased (randomly-generated) histogram distributions. Furthermore, a preliminary assessment of prime predictability is conducted on chronologically ordered NCBI genome snapshots over an 18-month period using an artificial neural network; three distinct supervised machine learning algorithms are used to train and test the system on customized NCBI data sets to forecast future prime states---revealing that, to a modest degree, it is feasible to make such predictions.
Category: Quantitative Biology
[15] viXra:1212.0041 [pdf] submitted on 2012-12-06 09:38:20
Authors: Aristotelis Kittas, Carito Guziolowski, Niels Grabe
Comments: 20 Pages.
We present a method to discover signaling pathways, quantify the relationship of preselected source/target nodes, and extract relevant subgraphs in large scale biological networks. This is demonstrated over the hepatocyte growth factor (HGF) stimulated cell migration and proliferation in a keratinocyte-fibroblast co-culture. The algorithm (MCWalk) is implemented with random walks using Monte Carlo simulations. We extract a master network by overlaying case specific microarray data from the NCI Pathway Interaction Database (PID) using a fully automatic pipeline without any manual network construction, and uncover the association of HGF receptor c-Met nodes, differentially expressed (DE) protein nodes and cellular states. We show that the network has a scale-free structure and identify key regulator nodes based on their random walk traversal frequency. This property is shown to be very weakly correlated to node degree, contrary to what is expected from similar centrality measures. The differences with standard methods, such as shortest-path, commonly used in the analysis of such networks are discussed and compared with this approach, highlighting important pathways which are exclusively obtained with our random walks algorithm.
Category: Quantitative Biology
[14] viXra:1210.0170 [pdf] submitted on 2012-10-28 21:00:28
Authors: Wan-Jiung Hu
Comments: 34 Pages.
Unstable angina is common clinical manifestation of atherosclerosis. However, the detailed pathogenesis of unstable angina is still not known. Here, I propose that unstable angina is a mixed TH17 and TH1 immune disorder. By using microarray analysis, I find out that TH1 and TH17 related cytokine, cytokine receptor, chemokines, complement, immune-related transcription factors, anti-bacterial genes, Toll-like receptors, and heat shock proteins are all up-regulated in peripheral leukocytes of unstable angina. In addition, H-ATPase, glycolytic genes, platelet and RBC related genes are also up-regulated in peripheral leukocytes of during unstable angina. It also implies that atherosclerosis is a mixed TH17 and TH1 autoimmune disease. If we know the etiology of unstable angina as well as atherosclerosis better, we can have better methods to control and prevent this detrimental illness.
Category: Quantitative Biology
[13] viXra:1205.0090 [pdf] submitted on 2012-05-23 02:08:11
Authors: Wan-Jiung Hu
Comments: 44 Pages.
Currently, there are two major theories for the pathogenesis of sepsis: hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine storm causes the symptoms of sepsis. On the contrary, hypoimmune theory suggests that immunosuppression causes the manifestations of sepsis. By using microarray study, this study implies that hyperactivity of TH17-like innate immunity and failure of adaptive immunity are noted in sepsis patients. Thus, both hyperimmune and hypoimmune play important roles in the pathophysiology of sepsis.
Category: Quantitative Biology
[12] viXra:1204.0090 [pdf] submitted on 2012-04-24 06:10:46
Authors: Wan-Jiung Hu
Comments: 18 Pages.
Acute Respiratory Distress Syndrome (ARDS) is a very severe syndrome leading to respiratory failure and subsequent mortality. Sepsis is the leading cause of acute respiratory distress syndrome. Thus, extracellular bacteria play an important role in the pathophysiology of ARDS. Overactivated neutrophils are the major effector cells in ARDS. Thus, extracellular bacteria triggered TH17 host immunity with neutrophil activation counts for the etiology of ARDS. Here, I use microarray analysis to describe TH17 related cytokine up-regulation in whole blood of ARDS patients. In addition, TGF-β secreting Treg cells play important roles in lung fibrosis. Thus, ARDS is actually a TH17 and Treg immune disorder.
Category: Quantitative Biology
[11] viXra:1204.0070 [pdf] submitted on 2012-04-16 20:55:43
Authors: Wan-Jiung Hu
Comments: 19 Pages.
Schizophrenia is a very common psychiatric disorder. However, its etiology and pathogenesis is still unknown. Current theory saying that neurotransmitter imbalance such as serotonin or dopamine only provides limited effectiveness in schizophrenia treatment by drugs changing serotonin and dopamine concentration. Despite of such treatment, majority of schizophrenia patients still have very poor prognosis. Thus, the neurotransmitter imbalance theory is not correct. Here, I propose that schizophrenia is actually a TH2 dominant autoimmune disorder. The candidate of autoantigen could be acetylcholine receptors of CNS. My theory can explain the positive as well as negative symptoms of schizophrenia. By microarray analysis of PBMCS, one-tenth of the total 519 significantly expressed genes are immune-related genes. Among them, TH2 related genes are significantly up-regulated including IL-4, histidine decarboxylase, aldehyde dehydrogenase, CCR9, IgE Fc receptor, GATA2, serotonin receptor, phospholipase A2, and prostaglandin D2 synthase. Besides, TH1 and TH17 related genes are down-regulated including CXCL5, cathepsin C, and neutrophil related S100 binding proteins. The new theory sheds a light to better control this detrimental illness. Anti-inflammatory agents could be used to manage schizophrenia in the near future.
Category: Quantitative Biology
[10] viXra:1202.0076 [pdf] submitted on 2012-02-24 14:46:48
Authors: Gregory Chaitin
Comments: 23 Pages.
In this paper we present an information-theoretic analysis of Darwin's theory of evolution, modeled as a hill-climbing algorithm on a fitness landscape. Our space of possible organisms consists of computer programs, which are subjected to random mutations. We study the random walk of increasing fitness made by a single mutating organism. In two different models we are able to show that evolution will occur and to characterize the rate of evolutionary progress, i.e., the rate of biological creativity.
Category: Quantitative Biology
[9] viXra:1112.0095 [pdf] submitted on 2011-12-31 15:35:48
Authors: Wen-sau Yim, Michael Harney
Comments: 14 Pages.
Cancer growth and decay can be modeled as a system of chaotic nonlinear differential equations. The system is based on a reaction-diffusion cancer growth model, expressed by a mathematical model that is simplified by Ivancevicet. al. This allows useful parameters to be applied for simulation and then recreated in C and Java, to directly compare with its predecessor project. A variation in a set of the parameters is found to decrease tumor growth in the early stages of tumor development.
Category: Quantitative Biology
[8] viXra:1110.0001 [pdf] submitted on 1 Oct 2011
Authors: Michael Harney
Comments: 6 pages
This paper describes a method of tracking the electromagnetic
dipole, with a three-dimensional representation of the dipole being
graphically displayed in real-time so as to provide diagnostic
information about a patient's heart. By knowing the coordinates
and orientation of the heart dipole and comparing this data with a
healthy heart, cardio-specialists may be able to determine where
damaged tissue is located or other diseases in progress.
Category: Quantitative Biology
[7] viXra:1106.0003 [pdf] submitted on 5 Jun 2011
Authors: Diego Lucio Rapoport
Comments: 16 pages
We reintroduce logophysics based on self-referential torsion fields and the Klein
bottle (KB) logic, which unifies the objective and subjective realms. We apply it to biology,
particularly allosterics and the genetic code. We reveal several topologies of the genetic
code and its bioinformatics codification, in particular the hyper Klein bottle (HKB) surface.
We relate it to the Universal Rewrite System, the Code of Nature, and Dirac algebra.We
find that the double helix is unnecessary in this setting, and elaborate the ontology of 3D
with regards to time, multistable perception, and a topological (lawless) form of Newton's
Third Law. We present the key ideas for a logophysical theory for contextual evolution.
Category: Quantitative Biology
[6] viXra:1103.0085 [pdf] submitted on 22 Mar 2011
Authors: Sergey V. Ershkov
Comments: 6 pages.
Here are presented a key points of new universal model for population evolution in
reactive environment: 1) generalization of the Logistic equation in the case of reactive
environment for population dynamics model in biology (also, for the model of exhaustion
of main resources in geology, or for filling of an ecological niches in ecology, or for
modeling of capacities of a proper markets in economics), 2) new type of asymptotic
solution for such an equation (which is tested on human population growth), 3) reduction
of such an equation to Abel ordinary differential equation in general case.
Category: Quantitative Biology
[5] viXra:1008.0004 [pdf] submitted on 3 Aug 2010
Authors: W. B. Vasantha Kandasamy, Florentin Smarandache, S. R. Kannan, S. Ramathilagam
Comments: 144 Pages.
The study of environmental pollution by chemicals used in
agriculture as pesticide or as fertilizers or pollution caused by
industries and chemical plants which use chemicals have not
been analysed systematically.
This book has five chapters. First chapter is introductory in
nature. Here we just study chemical pollution caused by
garment industries in chapter two of this book using fuzzy
associative memories.
Category: Quantitative Biology
[4] viXra:1005.0022 [pdf] submitted on 11 Mar 2010
Authors: W. B. Vasantha Kandasamy, Florentin Smarandache
Comments: 472 pages
Neutrosophic logic grew as an alternative to the existing
topics and it represents a mathematical model of uncertainty,
vagueness, ambiguity, imprecision, undefined-ness,
unknown, incompleteness, inconsistency, redundancy and
contradiction. Despite various attempts to reorient logic,
there has remained an essential need for an alternative
system that could infuse into itself a representation of the
real world. Out of this need arose the system of neutrosophy
and its connected logic, neutrosophic logic. This new logic,
which allows also the concept of indeterminacy to play a role
in any real-world problem, was introduced first by one of the
authors Florentin Smarandache.
Category: Quantitative Biology
[3] viXra:1004.0021 [pdf] submitted on 8 Mar 2010
Authors: Sreepurna Malakar, Florentin Smarandache, Sukanto Bhattacharya
Comments: 12 pages
This short technical paper advocates a bootstrapping algorithm from which we can form a
statistically reliable opinion based on limited clinically observed data, regarding whether
an osteo-hyperplasia could actually be a case of Ewing's osteosarcoma. The basic
premise underlying our methodology is that a primary bone tumour, if it is indeed
Ewing's osteosarcoma, cannot increase in volume beyond some critical limit without
showing metastasis. We propose a statistical method to extrapolate such critical limit to
primary tumour volume. Our model does not involve any physiological variables but
rather is entirely based on time series observations of increase in primary tumour volume
from the point of initial detection to the actual detection of metastases.
Category: Quantitative Biology
[2] viXra:1003.0132 [pdf] submitted on 6 Mar 2010
Authors: M. Khoshnevisan, Sukanto Bhattacharya, Florentin Smarandache
Comments: 14 pages
In this paper we propose a classification scheme to isolate truly benign tumors from those
that initially start off as benign but subsequently show metastases. A non-parametric
artificial neural network methodology has been chosen because of the analytical
difficulties associated with extraction of closed-form stochastic-likelihood parameters
given the extremely complicated and possibly non-linear behavior of the state variables.
This is intended as the first of a three-part research output. In this paper, we have
proposed and justified the computational schema. In the second part we shall set up a
working model of our schema and pilot-test it with clinical data while in the concluding
part we shall give an in-depth analysis of the numerical output and model findings and
compare it to existing methods of tumor growth modeling and malignancy prediction.
Category: Quantitative Biology
[1] viXra:0702.0027 [pdf] submitted on 25 Feb 2007
Authors: Alex Kaivarainen
Comments: recovered from sciprint.org
During many years our Laboratory of molecular biophysics was involved in study of
solvent dependent large-scale dynamics of proteins determined by relative thermal mobility of
their domains and subunits. The role of large-scale dynamics in the mechanism of protein
function, the signal transmission, allosteric effects and other water dependent effects in protein
solutions have been investigated.
Category: Quantitative Biology
[9] viXra:1205.0090 [pdf] replaced on 2012-06-12 09:22:14
Authors: Wan-Jiung Hu
Comments: 66 Pages.
Currently, there are two major theories for the pathogenesis of sepsis: hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine storm causes the symptoms of sepsis. On the contrary, hypoimmune theory suggests that immunosuppression causes the manifestations of sepsis. By using microarray study, this study implies that hyperactivity of TH17-like innate immunity and failure of adaptive immunity are noted in sepsis patients. I find out that innate immunity related genes are significantly up-regulated including CD14, TLR1,2,4,5,8, HSP70, CEBP proteins, AP1(JUNB, FOSL2), TGF-β, IL-6, TGF-α, CSF2 receptor, TNFRSF1A, S100A binding proteins, CCR2, formyl peptide receptor2, amyloid proteins, pentraxin, defensins, CLEC5A, whole complement machinery, CPD, NCF, MMP, neutrophil elastase, caspases, IgG and IgA Fc receptors(CD64, CD32), ALOX5, PTGS, LTB4R, LTA4H, and ICAM1. Majority of adaptive immunity genes are down-regulated including MHC related genes, TCR genes, granzymes/perforin, CD40, CD8, CD3, TCR signaling, BCR signaling, T & B cell specific transcription factors, NK killer receptors, and TH17 helper specific transcription factors(STAT3, RORA, REL). In addition, Treg related genes are up-regulated including TGFβ, IL-15, STAT5B, SMAD2/4, CD36, and thrombospondin. Thus, both hyperimmune and hypoimmune play important roles in the pathophysiology of sepsis.
Category: Quantitative Biology
[8] viXra:1205.0090 [pdf] replaced on 2012-06-10 20:13:06
Authors: Wan-Jiung Hu
Comments: 64 Pages.
Currently, there are two major theories for the pathogenesis of sepsis: hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine storm causes the symptoms of sepsis. On the contrary, hypoimmune theory suggests that immunosuppression causes the manifestations of sepsis. By using microarray study, this study implies that hyperactivity of TH17-like innate immunity and failure of adaptive immunity are noted in sepsis patients. I find out that innate immunity related genes are significantly up-regulated including CD14, TLR1,2,4,5,8, HSP70, CEBP proteins, AP1(JUNB, FOSL2), TGF-β, IL-6, TGF-α, CSF2 receptor, TNFRSF1A, S100A binding proteins, CCR2, formyl peptide receptor2, amyloid proteins, pentraxin, defensins, CLEC5A, whole complement machinery, CPD, NCF, MMP, neutrophil elastase, caspases, IgG and IgA Fc receptors(CD64, CD32), ALOX5, PTGS, LTB4R, LTA4H, and ICAM1. Majority of adaptive immunity genes are down-regulated including MHC related genes, TCR genes, granzymes/perforin, CD40, CD8, CD3, TCR signaling, BCR signaling, T & B cell specific transcription factors, NK killer receptors, and TH17 helper specific transcription factors(STAT3, RORA, REL). In addition, Treg related genes are up-regulated including TGFβ, IL-15, STAT5B, SMAD2/4, CD36, and thrombospondin. Thus, both hyperimmune and hypoimmune play important roles in the pathophysiology of sepsis.
Category: Quantitative Biology
[7] viXra:1205.0090 [pdf] replaced on 2012-06-03 09:52:38
Authors: Wan-Jiung Hu
Comments: 58 Pages.
Currently, there are two major theories for the pathogenesis of sepsis: hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine storm causes the symptoms of sepsis. On the contrary, hypoimmune theory suggests that immunosuppression causes the manifestations of sepsis. By using microarray study, this study implies that hyperactivity of TH17-like innate immunity and failure of adaptive immunity are noted in sepsis patients. Thus, both hyperimmune and hypoimmune play important roles in the pathophysiology of sepsis.
Category: Quantitative Biology
[6] viXra:1205.0090 [pdf] replaced on 2012-05-29 02:10:59
Authors: Wan-Jiung Hu
Comments: 57 Pages.
Currently, there are two major theories for the pathogenesis of sepsis: hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine storm causes the symptoms of sepsis. On the contrary, hypoimmune theory suggests that immunosuppression causes the manifestations of sepsis. By using microarray study, this study implies that hyperactivity of TH17-like innate immunity and failure of adaptive immunity are noted in sepsis patients. Thus, both hyperimmune and hypoimmune play important roles in the pathophysiology of sepsis.
Category: Quantitative Biology
[5] viXra:1204.0090 [pdf] replaced on 2012-05-10 03:03:16
Authors: Wan-Jiung Hu
Comments: 44 Pages.
Acute Respiratory Distress Syndrome (ARDS) is a very severe syndrome leading to respiratory failure and subsequent mortality. Sepsis is the leading cause of acute respiratory distress syndrome. Thus, extracellular bacteria play an important role in the pathophysiology of ARDS. Overactivated neutrophils are the major effector cells in ARDS. Thus, extracellular bacteria triggered TH17-like innate immunity with neutrophil activation counts for the etiology of ARDS. Here, I use microarray analysis to describe TH17-like innate immunity related cytokine including TGF-β and IL-6 up-regulation in whole blood of ARDS patients. Innate TH17 related TLR1,2,4,5,8, HSP70, G-CSF, GM-CSF, complements, defensin, PMN chemokines, cathepsins, Fc receptors, NCFs, FOS, JunB, CEBPs, NFkB, and leukotriene B4 are all up-regulated. TGF-β secreting Treg cells play important roles in lung fibrosis. Up-regulation of Treg associated STAT5B and TGF-β with down-regulation of MHC genes, TCR genes, and costimulation molecule CD86 are noted. Key TH17 transcription factors, STAT3 and RORα, are down-regulated. Thus, the full adaptive TH17 helper CD4 T cells may not be successfully triggered. Many fibrosis promoting genes are also up-regulated including MMP8, MMP9, FGF13, TIMP1, TIMP2, PLOD1, P4HB, P4HA1, PDGFC, HMMR, HS2ST1, CHSY1, and CSGALNACT. Failure to induce successful adaptive immunity could also attribute to ARDS pathogenesis. Thus, ARDS is actually a TH17-like and Treg immune disorder.
Category: Quantitative Biology
[4] viXra:1204.0090 [pdf] replaced on 2012-05-09 05:14:56
Authors: Wan-Jiung Hu
Comments: 44 Pages.
Acute Respiratory Distress Syndrome (ARDS) is a very severe syndrome leading to respiratory failure and subsequent mortality. Sepsis is the leading cause of acute respiratory distress syndrome. Thus, extracellular bacteria play an important role in the pathophysiology of ARDS. Overactivated neutrophils are the major effector cells in ARDS. Thus, extracellular bacteria triggered TH17 host immunity with neutrophil activation counts for the etiology of ARDS. Here, I use microarray analysis to describe TH17 innate immunity related cytokine including TGF-β and IL-6 up-regulation in whole blood of ARDS patients. Innate TH17 related TLR1,2,4,5,8, HSP70, G-CSF, GM-CSF, complements, defensin, PMN chemokines, cathepsins, Fc receptors, NCFs, STAT5B, FOS, JunB, CEBPs, NFkB, and leukotriene B4 are all up-regulated. TGF-β secreting Treg cells play important roles in lung fibrosis. Up-regulation of STAT5B and TGF-β with down-regulation of MHC genes, TCR genes, and costimulation molecule CD86 are noted. Many fibrosis promoting genes are also up-regulated including MMP8, MMP9, FGF13, TIMP1, TIMP2, PLOD1, P4HB, P4HA1, PDGFC, HMMR, HS2ST1, CHSY1, and CSGALNACT. Failure to induce successful adaptive immunity could also attribute to ARDS pathogenesis. Thus, ARDS is actually a TH17 and Treg immune disorder.
Category: Quantitative Biology
[3] viXra:1204.0090 [pdf] replaced on 2012-05-04 07:52:09
Authors: Wan-Jiung Hu
Comments: 39 Pages.
Acute Respiratory Distress Syndrome (ARDS) is a very severe syndrome leading to respiratory failure and subsequent mortality. Sepsis is the leading cause of acute respiratory distress syndrome. Thus, extracellular bacteria play an important role in the pathophysiology of ARDS. Overactivated neutrophils are the major effector cells in ARDS. Thus, extracellular bacteria triggered TH17 host immunity with neutrophil activation counts for the etiology of ARDS. Here, I use microarray analysis to describe TH17 related cytokine up-regulation in whole blood of ARDS patients. In addition, TGF-β secreting Treg cells play important roles in lung fibrosis. Thus, ARDS is actually a TH17 and Treg immune disorder.
Category: Quantitative Biology
[2] viXra:1204.0090 [pdf] replaced on 2012-05-03 08:23:33
Authors: Wan-Jiung Hu
Comments: 34 Pages.
Acute Respiratory Distress Syndrome (ARDS) is a very severe syndrome leading to respiratory failure and subsequent mortality. Sepsis is the leading cause of acute respiratory distress syndrome. Thus, extracellular bacteria play an important role in the pathophysiology of ARDS. Overactivated neutrophils are the major effector cells in ARDS. Thus, extracellular bacteria triggered TH17 host immunity with neutrophil activation counts for the etiology of ARDS. Here, I use microarray analysis to describe TH17 related cytokine up-regulation in whole blood of ARDS patients. In addition, TGF-β secreting Treg cells play important roles in lung fibrosis. Thus, ARDS is actually a TH17 and Treg immune disorder.
Category: Quantitative Biology
[1] viXra:1103.0085 [pdf] replaced on 2012-05-19 03:51:43
Authors: Sergey V. Ershkov
Comments: 7 Pages. Keywords: Logistic equation; evolution of population; prognosis of Human population; reactive environment; catastrophes theory; Abel ODE
Here are presented a key points of new universal model for evolution of population in reactive environment: 1) generalization of the Logistic equation to the case of reactive environment for models of population dynamics in biology (also, for the model of exhaustion of main resources in geology, or for filling of an ecological niches in ecology, or for modeling of the capacities of a proper markets in economics), 2) new type of asymptotic solution for such equation (which is tested on human population growth), 3) reduction of such an equation to Abel ODE in general case.
Category: Quantitative Biology