TY - JOUR. T1 - Glycosyl-phosphatidylinositol (GPI)-anchored membrane association of the porcine reproductive and respiratory syndrome virus GP4 glycoprotein and its co-localization with CD163 in lipid rafts. AU - Du, Yijun. AU - Pattnaik, Asit K.. AU - Song, Cheng. AU - Yoo, Dongwan. AU - Li, Gang. PY - 2012/3/1. Y1 - 2012/3/1. N2 - The porcine reproductive and respiratory syndrome virus (PRRSV) glycoprotein 4 (GP4) resembles a typical type I membrane protein in its structure but lacks a hydrophilic tail at the C-terminus, suggesting that GP4 may be a lipid-anchored membrane protein. Using the human decay-accelerating factor (DAF; CD55), a known glycosyl-phosphatidylinositol (GPI) lipid-anchored protein, chimeric constructs were made to substitute the GPI-anchor domain of DAF with the putative lipid-anchor domain of GP4, and their membrane association and lipase cleavage were determined in cells. The DAF-GP4 fusion protein was transported to the plasma membrane and was cleaved by ...
Decay-accelerating factor (DAF), extracted from the stroma of human erythrocytes, was purified to homogeneity and incorporated into the membrane of sheep red cell complement intermediates, where its functional properties were analyzed. Incorporation of DAF into the cell membranes was temperature dependent, took place on pronase- or trypsin-treated erythrocytes, and did not depend on prior deposition of antibody, C1 or C4. Serum lipoproteins (high and low density) effectively inhibited DAF incorporation, but had no effect on the activity of DAF after its association with the cell membrane. The incorporated DAF could not be removed from the red cell surface by repeated washings in the presence of high salt concentration but was solubilized when the stroma were extracted with 0.1% Nonidet P-40. The presence of DAF in the membrane of EA did not affect the deposition of C1 and C4, but as few as 10(2) DAF molecules per cell profoundly inhibited the assembly of C3 and C5 convertases of both the ...
Decay-accelerating factor (DAF) is a 70,000 Mr protein that has been isolated from the membrane of red cells. The function of DAF is to inhibit the assembly of amplifying enzymes of the complement cascade on the cell surface, thereby protecting them from damage by autologous complement. We raised monoclonal antibodies to DAF and used them to study its distribution in cells from the peripheral blood of normal individuals and of patients with paroxysmal nocturnal hemoglobinuria (PNH), a disease characterized by the unusual susceptibility of red cells to the hemolytic activity of complement. The results of immunoradiometric assays and of fluorescence-activated cell sorter analysis showed that DAF was present not only on red cells but was widely distributed on the surface membrane of platelets, neutrophils, monocytes, and B and T lymphocytes. By Western blotting, we observed small but consistent differences in the Mr of DAF from the membranes of various cell types. Quantitative studies showed that ...
Clone REA300 recognizes the CD55 antigen, a glycoprotein also known as complement decay-accelerating factor (DAF). There are two mouse CD55 genes, which share 85% nucleotide and 78% amino acid identities, and have been designated CD55-glycosylphosphatidylinositol and CD55-transmembrane to reflect the two alternate mechanisms of membrane attachment. Both proteins are recognized by clone REA300. CD55 is broadly distributed among hematopoietic and non-hematopoietic cells. It is expressed on the plasma membranes of all cell types that are in intimate contact with serum and it is also found on the surfaces of epithelial cells, lining extracellular compartments. CD55 plays multiple physiologic roles including tissue protection from the cytotoxic complement injury, anti-inflammatory function owing to its anti-adherence properties which enhance transmigration of monocytes and macrophages and reduce tissue injury. CD55 plays an essential role during pregnancy and is involved in the protection of the
CRP seems to be not only a biomarker for atherosclerosis but also a mediator of plaque formation.3 By binding to enzymatically degraded low-density lipoprotein, CRP is able to activate the classical pathway of complement,13 serving as a potential link between complement activation and atherosclerosis.9,10 To protect against complement-mediated cell lysis, nucleated cells express complement inhibitor proteins on their surface. By upregulating the expression of these proteins in endothelial cells, CRP may serve to protect ECs from complement-mediated injury.. The ability of CRP to bind to nucleated cells and cause complement activation without cytolysis14 has been largely attributed to its ability to recruit the inhibitory plasma protein factor H.15 However, our results indicate that CRP may play a more active, protective role by stimulating the expression of DAF, CD46, and CD59 in endothelial cells. The kinetics of DAF expression were analyzed in greater detail because DAF seems to be the most ...
The kidney is particularly susceptible to complement-mediated injury in a number of clinical settings, and congenital deficiency or defects in the complement-regulatory proteins MCP and factor H are strongly associated with the development of renal disease. In the current study, we demonstrated that Crry (the murine homolog of MCP in the kidney) is the only membrane-bound regulator of complement expressed by murine TECs. Crry is expressed on the cell membrane, and its expression is concentrated in the basolateral portion of the cell. Polarized TECs regulate complement more efficiently on the basolateral surface of the cells than on the apical surface, in part because of Crry expression at this site. As with renal ischemia/reperfusion (I/R) (21), chemical hypoxia of the TECs causes a reduction in surface Crry levels, and the distribution within the cell is also altered.. Spontaneous complement activation on the surface of TECs is also controlled by endogenous factor H. When rH 19-20 was added to ...
Decay-accelerating factor (CD55), a regulator of the alternative and classical pathways of complement activation, is expressed on all serum-exposed cells. It is used by pathogens, including many enteroviruses and uropathogenic Escherichia coli, as a receptor prior to infection. We describe the x-ray structure of a pathogen-binding fragment of human CD55 at 1.7 A resolution containing two of the three domains required for regulation of human complement. We have used mutagenesis to map biological functions onto the molecule; decay-accelerating activity maps to a single face of the molecule, whereas bacterial and viral pathogens recognize a variety of different sites on CD55.
Clone REA678 recognizes the mouse CD97 antigen variant 2 (CD97v2).CD97 is a member of the EGF-TM7 family, which is a group of class II seven-span transmembrane receptors expressed ubiquitously, but mainly expressed by cells of the immune system. CD97 has seven putative transmembrane domains. It has an extended extracellular segment containing several adhesion molecule structure motifs, and has been shown to interact with the human DAF (CD55). The variant 2 of CD97 exhibits a 94 aa deletion that results in loss of the third EGF-like repeat. Additional information: Clone REA678 displays negligible binding to Fc receptors. - USA
Simpson, R. J., Guy, K., Whyte, G. P., & Florida-James, G. D. (2005). Lymphocyte Apoptosis, Adhesion/activation Molecules And Complement Regulatory Proteins Following Intensive, Moderate And Eccentric Exercise: 1739 11:30 AM ??? 11:45 AM. Medicine and science in sports and exercise, 37(Supplement), (S336). doi:10.1097/00005768-200505001-01738. ISSN 0195-9131. ...
Simpson, R. J., Guy, K., Whyte, G. P., & Florida-James, G. D. (2005). Lymphocyte Apoptosis, Adhesion/activation Molecules And Complement Regulatory Proteins Following Intensive, Moderate And Eccentric Exercise: 1739 11:30 AM ??? 11:45 AM. Medicine and science in sports and exercise, 37(Supplement), (S336). doi:10.1097/00005768-200505001-01738. ISSN 0195-9131. ...
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Vol 21: Study of Coxsackie B viruses interactions with Coxsackie Adenovirus receptor and Decay-Accelerating Factor using Human CaCo-2 cell line.. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
The objective of our study was the investigation of differential pathways in cardiac and skeletal muscles that protect one tissue and render the other susceptible to damage within a single organism. This approach might help to identify relevant pathways and possible candidates for therapeutic intervention. Dysferlin-deficient muscular dystrophy appeared to be a suitable model for this approach, because dysferlin is expressed in skeletal and cardiac muscles, but, clinically, the heart is thought to be unaffected in LGMD2B (25, 26). We demonstrate down-regulation of DAF/CD55 on mRNA and protein levels in dysferlin-deficient mice and LGMD2B patients, leading to activation of the MAC of the complement cascade on skeletal muscle cells. In vitro, dysferlin-deficient human myotubes are highly susceptible to complement attack, whereas normal human myoblasts/myotubes are not (19). The underlying mechanism appears to be a lack of myostatin, leading to down-regulation of SMAD proteins, with a negative ...
TY - JOUR. T1 - Decay accelerating factor regulates complement activation on glomerular epithelial cells. AU - Quigg, R. J.. AU - Nicholson-Weller, A.. AU - Cybulsky, A. V.. AU - Badalamenti, John. AU - Salant, D. J.. PY - 1989. Y1 - 1989. N2 - Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
During sublytic complement attack on human neutrophils, plasma-membrane vesicles are shed from the cell surface as a cell-protection mechanism. By using surface-iodinated neutrophils it was found that less than 2% of surface label was recovered in shed vesicles under conditions where 40% of complement component C9 was shed. SDS/PAGE of 125I-labelled shed vesicles and plasma membranes showed differences in iodination pattern, demonstrating the sorting of membrane proteins into the shed vesicles. Analysis of 32P-labelled phospholipids after labeling of neutrophils with [32P]Pi before sublytic complement attack showed the presence of phosphatidic acid, phosphatidylcholine, phosphatidyl-ethanolamine, phosphatidylinositol and polyphosphoinositides in shed vesicles. Quantitative analysis using [3H]acetic anhydride-labelling method showed that the molar proportions of phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and sphingomyelin were the same in shed vesicles as in plasma ...
Membrane cofactor protein (MCP) is a complement regulatory protein that is expressed on human cells and cell lines as two relatively broad species with Mr of 58,000-68,000 and 48,000-56,000. The structure of a previously reported cDNA clone indicated that MCP was a type 1 membrane glycoprotein and a member of the regulators of complement activation gene/protein cluster. However, it did not provide an explanation for the unusual phenotypic pattern of MCP. Therefore, in parallel with an analysis of the gene, additional cDNAs were cloned and characterized. Six different MCP cDNA classes were identified. All encode the same 5 untranslated signal peptide, four SCRs, transmembrane domain, and basic amino acid anchor. However, they differ in the length and composition of an extracellular serine/threonine/proline (STP)-rich area, a site of heavy O-glycosylation, and cytoplasmic tail. Analysis of the MCP gene demonstrated that the variation in cDNA structure was a result of alternative splicing. ...
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Inhabit shallow gravel riffles, sometimes rocky runs and pools, of headwaters, creeks and small rivers (Ref. 5723); also found in streams (Ref. 10294). Adults feed on midge and blackfly larvae, mayfly nymphs, isopods, amphipods, and caddisfly larvae (Ref. 10294). Distinct pairing during breeding (Ref. 36980). Eggs are found buried in the substrate (Ref. 7043). ...
Results Brain pathological injury was the most serious at 24 h after reperfusion, The complement regulatory protein CD46 expression decreased gradually after local cerebral ischaemia-reperfusion injury, the lowest at 24 h after reperfusion, and returned to normal at 96 h after reperfusion.complement regulatory protein CD46 expression was negative correlated with brain pathological injury.. ...
Inherited deficiencies of several complement components strongly predispose to systemic lupus erythematosus (SLE) while deficiencies of complement inhibitors are found in kidney diseases such as atypical hemolytic uremic syndrome (aHUS). The exons of complement inhibitor genes CD46 and CFH (factor H) were fully sequenced using the Sanger method in SLE patients with nephritis originating from two cohorts from southern and mid Sweden (n = 196). All identified mutations and polymorphisms were then analyzed in SLE patients without nephritis (n = 326) and in healthy controls (n = 523). We found nonsynonymous, heterozygous mutations in CFH in 6.1% patients with nephritis, in comparison with 4.0% and 5.4% in patients without nephritis and controls, respectively. No associations of SLE or nephritis with common variants in CFH (V62I/Y402H/E936D) were found. Furthermore, we found two nonsynonymous heterozygous mutations in CD46 in SLE patients but not in controls. The A353V polymorphism, known to affect function
Membrane cofactor protein (MCP), a regulatory molecular of the complement system with cofactor activity for the factor I-mediated inactivation of C3b and C4b, is widely distributed, being present on leukocytes, platelets, endothelial cells, epithelial cells, and fibroblasts. MCP was purified from a human T cell line (HSB2) and the NH2-terminal 24-amino acid sequence obtained by Edman degradation. An oligonucleotide probe based on this sequence was used to identify a clone from a human monocytic (U937) cDNA library. Nucleotide sequencing showed a 43-bp 5-untranslated region, an open reading frame of 1,152 bp, and a 335-bp 3-untranslated region followed by a 16-bp poly(A) track. The deduced full-length MCP protein consists of a 34-amino acid signal peptide and a 350-amino acid mature protein. The protein has, beginning at the NH2 terminus, four approximately 60-amino acid repeat units that match the consensus sequence found in a multigene family of complement regulatory proteins (C3b-receptor or ...
Background/Purpose: The influence of complement-mediated innate immune responses on cartilage and bone homeostasis in the ageing joint have not been studied. Inappropriate complement-mediated cell damage is prevented by membrane regulators such as CD59. Synovial tissue expression of CD59 is altered during inflammatory arthritis; elevated CD59 levels may be necessary to protect joint tissues. Roles of CD59 in maintaining tissue equilibrium and structural architecture within the synovial joint have not been described previously. Since CD59a is the primary regulator of membrane attack complex assembly in mice; we used CD59a-gene-deleted mice (CD59a-/-) as tools to unravel the function of CD59a in modulating age-related joint degeneration. Methods: Hind limbs were collected from C57BL/6J wild type (WT) and CD59a-/- mice at 8-, 20- and 50- weeks of age (6 to 10 mice/group). The Mankin score was used to classify the histopathological severity of osteoarthritic (OA) lesions. Three dimensional ...
CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone SPM616 ] validated in IHC, IF, FC (AH12772-100), Abgent
Myocarditis is a cardiac disease associated with inflammation and injury of the myocardium. It results from various etiologies, both noninfectious and infectious, but coxsackievirus B3 (CVB3) is still considered the dominant etiological agent. Myocarditis may be caused by direct cytopathic effects of virus, a pathologic immune response to persistent virus, or autoimmunity triggered by the viral infection. The virus enters the myocyte through internalization of the coxsackie-adenoviral receptor (CAR) and its coreceptor, decay-accelerating factor (DAF). Viral proteases cleave various proteins in the host cell. One example is viral protease 2A, which cleaves eukaryote initiation factor 4G (eIF4G) and the dystrophin protein, resulting in a complete shutdown of cap-dependent RNA translation and cytoskeletal destruction in infected cardiomyocytes, respectively. CVB3 also cleaves the member of the Bcl-2 family Bid, leading to apoptosis. CVB3 infection also induces the cleavage of cyclin D protein ...
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Homo sapiens membrane cofactor protein (CD46, trophoblast-lymphocyte cross-reactive antigen) (MCP), transcript variant h, mRNA. (H00004179-R27) - Products - Abnova
Homo sapiens membrane cofactor protein (CD46, trophoblast-lymphocyte cross-reactive antigen) (MCP), transcript variant n, mRNA. (H00004179-R17) - Products - Abnova
WWII German DAF Standarte-(aka German Labor Front, Deutsche Arbeitsfront) This is double sided and sewn on both side. Each color is a separate layer of sewn cloth including white border for cog, black cog wheel, white disk, and black swastika. There is a sewn sleeve on one edge for pole. A 6-in x 9-in brown patch, u
این مطالعه با هدف ارزیابی عملکرد سیستم لجن‌فعال هوادهی گسترده مورد استفاده برای تصفیه فاضلاب مجتمع پتروشیمی تبریز انجام شده است. سیستم تصفیه شامل آشغالگیر، API، متعادل‌سازی، انعقاد و لخته‌سازی، سیستم DAF، حوض هوادهی، زلال‌ساز اولیه و ثانویه و فیلتراسیون می‌باشد. این تصفیه‌خانه جهت تصفیه فاضلاب صنعتی تولیدی از واحدهای مختلف مجتمع و با هدف استفاده مجدد از پساب تصفیه شده، طراحی شده است. جهت ارزیابی عملکرد تصفیه‌خانه، نمونه‌های ترکیبی 12 ساعته متناسب با دبی در 4 نوبت در طی 6 ماه برداشته شده و پارامترهای COD، BOD5، TDS، TSS، فنل، سیانید، روغن، آمونیاک و TKN مطابق با
TY - JOUR. T1 - Assessing donor chimerism using flow cytometry in paroxysmal nocturnal haemoglobinuria after stem cell transplantation--a case report.. AU - Raja Sabudin, Raja Zahratul Azma. AU - Hussin, Noor Hamidah. AU - Chooi Fun, Leong. AU - Ainoon, O.. AU - Cheong, S. K.. PY - 2006/12. Y1 - 2006/12. N2 - Paroxysmal nocturnal haemoglobinuria (PNH) is an acquired haemopoietic stem cell disorder arising from somatic mutation of the X-linked PIG-A gene which leads to deficiency of the glycosylphosphatidylinositol (GP1) membrane anchor proteins such as CD 59 (MIRL: membrane inhibitor of reactive lysis) and CD 55 (DAF: decay accelerating factor). Allogeneic peripheral blood stem cell transplant (PBSCT) is a curative mode of treatment in symptomatic PNH patients. Assessment of donor chimerism for PBSCT can be performed by various methods including short tandem repeat loci (STR) and variable number of tandem repeats (VNTR). Flow cytometry, which is much cheaper and faster, also can be used to ...
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RHEUMATOID ARTHRITIS. Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects mainly diarthrodial joints and periarticular structures, and can acquire a systemic character. Rheumatoid arthritis affects approximately 1% of the world population, being two to three times more common in women.1. The etiology of RA has not been completely clarified. However, environmental and genetic factors have contributed to the development of the disease. In the early stages of RA, proliferation and edema of the synovial layer cells occur, with infiltration of B and T cells, macrophages, and granulocytes. The synovium thickens, and the joint becomes swollen and painful. With progression, synovial proliferation leads to the formation of pannus, a tissue that invades the articular cartilage and bone. Joint destruction is irreversible. Osteoclasts reabsorb bone, and there is release of proteolytic enzymes, such as metal-loproteinases, aggrecanases, and cathepsins, responsible for the destruction of ...
NEW HAVEN, Conn.--(BUSINESS WIRE)--Alexion Pharmaceuticals, Inc. (NASDAQ:ALXN) today announced the initiation of two Phase 3 trials of ALXN1210, a highly innovative, longer-acting anti-C5 antibody that inhibits terminal complement. The first trial is a Phase 3 open-label, multinational, active-controlled study of ALXN1210 compared to eculizumab (Soliris®) in complement inhibitor treatment-naïve patients with paroxysmal nocturnal hemoglobinuria (PNH).
... is established by flow cytometric analysis of CD55 and CD59 on leukocytes and erythrocytes.
Paroxysmal nocturnal haemoglobinuria (PNH) is a unique disorder in which a substantial proportion of the patients red cells have an abnormal susceptibility to activated complement. This results from the presence of a clone that originates from a haematopoietic stem cell bearing an acquired somatic mutation in the X-linked gene ...
Learn about paroxysmal nocturnal hemoglobinuria. What are the symptoms, the causes and how to treat this condition? What can we do to cope...
Feldman L. Triiodothyronine (T3) toxicosis and paroxysmal nocturnal hemoglobinuria: report of case. J Am Osteopath Assoc 1981;80(7):491. doi: 10.7556/jaoa.1981.80.7.491.. Download citation file:. ...
1ERG: THREE-DIMENSIONAL SOLUTION STRUCTURE OF THE EXTRACELLULAR REGION OF THE COMPLEMENT REGULATORY PROTEIN, CD59, A NEW CELL SURFACE PROTEIN DOMAIN RELATED TO NEUROTOXINS
陣發性夜間血紅素尿症(paroxysmal nocturnal haemoglobinuria, PNH)是一種罕見的造血幹細胞疾病,因後天基因突變而造成[1]。一般來說,正常紅血球的細胞膜上有幾種保護性蛋白質,例如:蛋白衰變加速因子(decay accelerating factor, CD55)以及溶解細胞膜抑制物(membrane inhibitor of reactive lysis, CD59),使紅血球不會因補體(免疫系統的一部分)的攻擊而破裂[1]。然而,PNH患者因為在X染色體上的phosphatidylinositol glycan A (PIG-A)基因發生突變,造成某些醣脂質,例如glycosylphosphatidylinositols (GPI)無法形成,而使紅血球上的保護性蛋白質無法藉著GPI結合在紅血球的細胞膜上[1]。紅血球沒有這些蛋白質的保護就容易因人體內補體系統的攻擊而破裂,引起持續、慢性的血管內溶血性疾病,這也是造成疾病症狀及後續嚴重併發症的原因[2-4 ...
Speaking with your healthcare team about your condition and finding out what you can about the disease can be empowering and can help you understand how best to move forward. OneSource is a complimentary, personalized patient support program offered by Alexion, and tailored to the specific needs of people living with aHUS, gMG, HPP, LAL-D, NMOSD and PNH. Were here to help you learn, and were here to help you understand the options available to you.. ...
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Quantity100 testsVolume0.4ImmunogenHuman Acute Lymphocytic Leukemia (ALL) T cellsBackground InformationCD46 (MCP; membrane cofactor protein) is a m...
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