TY - JOUR. T1 - Clinical and Hematologic Benefits of Partial Splenectomy for Congenital Hemolytic Anemias in Children. AU - Rice, Henry E.. AU - Oldham, Keith T.. AU - Hillery, Cheryl A.. AU - Skinner, Michael A.. AU - OHara, Sara M.. AU - Ware, Russell E.. PY - 2003/2. Y1 - 2003/2. N2 - Objective: To assess the role of partial splenectomy for symptomatic children with various congenital hemolytic anemias. Summary Background Data: The use of total splenectomy for symptomatic children with congenital hemolytic anemias is restricted by concern of postsplenectomy sepsis. A partial splenectomy is an alternative procedure, although its utility remains incompletely defined. Methods: This longitudinal cohort study followed 25 symptomatic children with various congenital anemias who underwent partial splenectomy. Sixteen children had hereditary spherocytosis (HS), and nine children had other erythrocyte disorders. Outcome measures were clinical and laboratory hemolysis, splenic phagocytic and immune ...
Hematologic outcomes after total splenectomy and partial splenectomy for congenital hemolytic anemia., Brian R Englum, Jennifer Rothman, Sarah Leonard, Audra Reiter, Courtney Thornburg, Mary Brindle, Nicola Wright, Matthew M Heeney, C Jason Smithers, Rebeccah L Brown, Theodosia Kalfa, Jacob C Langer, Michaela Cada, Keith T Oldham, J Paul Scott, Mukta Sharma, Andrew M Davidoff, Kerri Nottage, Kathryn Bernabe, David B Wilson, Sanjeev Dutta, Bertil Glader, Shelley E Crary, Melvin S Dassinger, Levette Dunbar, Saleem Islam, Manjusha Kumar, Fred Rescorla, Steve Bruch, Andrew Campbell, Mary Austin, Robert Sidonio, Martin L Blakely, Henry E Rice, Splenectomy in Congenital Hemolytic Anemia Consortium, and Shawn D. St Peter. ...
Definition : Molecular assay reagents intended to identify mutations in the glucose-6-phosphate dehydrogenase (G6PD) gene, located at chromosome Xq28, which encodes for the glucose-6-phosphate dehydrogenase enzyme. Mutations at this locus have been identified in patients with congenital hemolytic anemia caused by G6PD deficiency.. Entry Terms : Anemia Gene Mutation Detection Reagents , Hemolytic Anemia Gene Mutation Detection Reagents , Congenital Hemolytic Anemia Gene Mutation Detection Reagents , G6PD Gene Mutation Detection Reagents , Reagents, Molecular Assay, Gene Anomaly, Mutation, G6PD. UMDC code : 24435 ...
How is R-type pyruvate kinase abbreviated? R-PK stands for R-type pyruvate kinase. R-PK is defined as R-type pyruvate kinase rarely.
Hereditary hemolytic anemia, a dominantly transmitted disorder, has affected 12 family members spanning three generations. The concentration of adenosine triphosphate in the red cells was about half that of comparably reticulocyte-rich blood. Since adenosine deaminase and adenosine kinase compete for a common substrate, the greatly increased activity of the former may interfere with nucleotide salvage via the latter. ...
The etiology of severe hemolytic anemia in most patients with recessive hereditary spherocytosis (rHS) and the related disorder hereditary pyropoikilocytosis (HPP) is unknown. Whole-exome sequencing of DNA from probands of 24 rHS or HPP kindreds identified numerous mutations in erythrocyte membrane α-spectrin (SPTA1). Twenty-eight mutations were novel, with null alleles frequently found in trans to missense mutations. No mutations were identified in a third of SPTA1 alleles (17/48). WGS revealed linkage disequilibrium between the common rHS-linked αBH polymorphism and a rare intron 30 variant in all 17 mutation-negative alleles. In vitro minigene studies and in vivo splicing analyses revealed the intron 30 variant changes a weak alternate branch point (BP) to a strong BP. This change leads to increased utilization of an alternate 3′ splice acceptor site, perturbing normal α-spectrin mRNA splicing and creating an elongated mRNA transcript. In vivo mRNA stability studies revealed the newly ...
The classic laboratory finding of hemolysis is anemia with an elevated reticulocyte count. The reticulocytosis reflects normal bone marrow function and occurs in response to the premature RBC destruction; reticulocytes are larger than older erythrocytes and have a blue-purple color known as polychromasia (Fig. 433-1). Reticulocytosis generally occurs 3 to 5 days after a sudden drop in hemoglobin concentration but is relatively constant in children with congenital hemolytic anemia. Making the diagnosis of hemolytic anemia begins with recognizing the constellation of signs and symptoms, then obtaining a complete blood count with reticulocyte count, and finally examining the peripheral blood smear. Additional laboratory findings supporting the diagnosis of hemolysis include elevated total serum bilirubin and lactate dehydrogenase (LDH; LDH being released from RBCs during hemolysis). Intravascular hemolysis also causes decreased or undetectable levels of haptoglobin, but this test is not specific so ...
Any one of a group of congenital hemolytic anemias in which there is no abnormal hemoglobin or spherocytosis and in which there is a defect of glycolysis in the erythrocyte. Common causes include deficiencies in GLUCOSE-6-PHOSPHATE ISOMERASE; PYRUVATE KINASE; and GLUCOSE-6-PHOSPHATE DEHYDROGENASE.
Purpose: The purpose of this study was to define the hematologic response to total splenectomy (TS) or partial splenectomy (PS) in children with hereditary spherocytosis (HS) or sickle cell disease (SCD). Methods: The Splenectomy in Congenital Hemolytic Anemia (SICHA) consortium registry collected hematologic outcomes of children with CHA undergoing TS or PS to 1 year after surgery. Using random effects mixed modeling, we evaluated the association of operative type with change in hemoglobin, reticulocyte counts, and bilirubin. We also compared laparoscopic to open splenectomy. Results: The analysis included 130 children, with 62.3% (n = 81) undergoing TS. For children with HS, all hematologic measures improved after TS, including a 4.1 g/dl increase in hemoglobin. Hematologic parameters also improved after PS, although the response was less robust (hemoglobin increase 2.4 g/dl, p , 0.001). For children with SCD, there was no change in hemoglobin. Laparoscopy was not associated with differences ...
The first chapter, by Dr. Dzik, is a real treat to read. Of special note is his critical analysis of the three common assumptions: (1) Abnormal results of commonly used laboratory tests such as prothrombin time, activated partial thromboplastin time, or platelet count have predictive value to identify which patients to treat; (2) blood components administered before procedures effectively correct hemostatic abnormalities; and (3) prophylactic transfusions preprocedure are of greater benefit than therapeutic transfusions after the procedure. The rest of the chapters in the first section provide a comprehensive overview of transfusion practices in common clinical conditions such as autoimmune hemolytic anemia, congenital hemolytic anemia, acquired hemolytic anemia, congenital coagulopathies, solid organ transplantation, hematopoietic stem cell transplantation, therapeutic apheresis, and the pediatric population. Although each of the distinguished authors adds his or her own flavor to the chapters, ...
An increase in circulating RETICULOCYTES, which is among the simplest and most reliable signs of accelerated ERYTHROCYTE production. Reticulocytosis occurs during active BLOOD regeneration (stimulation of red bone marrow) and in certain types of ANEMIA, particularly CONGENITAL HEMOLYTIC ANEMIA ...
A group of familial congenital hemolytic anemias characterized by numerous abnormally shaped erythrocytes which are generally spheroidal. The erythrocytes have increased osmotic fragility and are abnormally permeable to sodium ions.
This chapter is focused on the effect of natural products in pure form or characterized phytoconstituents on particularly inhibition of hemoglobin polymerization.This summarized information will be benecial for further exploration of new therapeutics in the treatment arena of SCA.Millions of people around the world, especially children, have been affected by SCA. This global burden is a growing concern nowadays as the yearly increase of newborns with SCA is expected from around three to four lakhs between and. SCA, congenital hemolytic anemia, is caused by a single amino acid substitution. This shows the way for polymerization of deoxygenated sickle hemoglobin which is the crucial step in the molecular pathogenesis of SCA.This polymerization alters the RBC rheology by changing its surface property, membrane damage, and dehydration of RBC.Potassium chloride cotransport and calciumactivated potassium efux are generally involved during the process of RBC dehydration. During this process, shape of ...
Inherited in a dominant and recessive manner. And each of these options is characterized by the presence of fetal hemoglobin. The most severe disease is considered to be a big thalassemia, which is expressed already in the neonatal period and ending fatally. Asymptomatic forms are due to the presence of HbA, HbF, and others formed early appearance of the child: tower skull, wide-set eyes, broad flat nose. There is an increase in the abdomen as a result of increased parenchymal organs, primarily the spleen ...
Thirteen Cases of Erythrocyte Pyruvate Kinase Deficiency Associated with Hereditary Hemolytic Anemia:-Clinical and Biochemical Studies- (1981 ...
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene is a mechanically-activated ion channel that links mechanical forces to biological signals. The encoded protein contains 36 transmembrane domains and functions as a homotetramer. Defects in this gene have been associated with dehydrated hereditary stomatocytosis. [provided by RefSeq, Jul 2015 ...
www.precisionpiezo.co.uk are pleased to announce the beta/early bird version of the Piezo20 hotend z-probe. SEE IT WORKING HERE Youve probably seen the extensive work on piezo electric sensing here on the forum. Weve made a unit which is ready to use with your groovemount hotend. The sensor modul
www.precisionpiezo.co.uk are pleased to announce the beta/early bird version of the Piezo20 hotend z-probe. SEE IT WORKING HERE Youve probably seen the extensive work on piezo electric sensing here on the forum. Weve made a unit which is ready to use with your groovemount hotend. The sensor modul
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In a parallel-kinematic, multi-axis system, all actuators act directly on a single moving platform. This means that all axes can be designed with identical dynamic properties, thus reducing the moved mass considerably. Hexapods are used for moving and precision positioning, aligning and displacing loads in all six degrees of freedom, i.e., three linear and three rotational axes ...
Fast, piezo-based scanners operate with the necessary velocities in the video frequency range for image stabilization and microscanning.
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The Online Mendelian Inheritance in Man (OMIM) compendium of human genes and genetic phenotypes includes three types of congenital dyserythropoietic anemia as reported in Table 1. A comprehensive overview of these disorders has been published recently.1. Congenital dyserythropoietic anemia type II is the most common of these inherited disorders. Typical morphological abnormalities of this condition are shown in Figure 1: these abnormalities clearly indicate that incomplete cytokinesis is one of the key features of erythroid cells in this condition.. More than 30 years ago, we investigated the pathophysiology of anemia in patients with congenital dyserythropoietic anemia type II in studies of iron kinetics.2 A wide variation in effectiveness of erythroid activity was observed, and a significant inverse relationship was found between ineffective erythropoiesis and peripheral hemolysis. In 4 patients with prominent peripheral hemolysis, splenectomy was carried out. Marked improvement in their ...
Congenital dyserythropoietic anemia type II (CDA II), or hereditary erythroblastic multinuclearity with positive acidified serum lysis test (HEMPAS) is a rare genetic anemia in humans characterized by hereditary erythroblastic multinuclearity with positive acidified serum lysis test. CDA type II is caused by mutations in the SEC23B gene. This gene provides instructions for making a protein that is involved in the transport of other proteins within cells. During the development of red blood cells, this protein may help ensure that proteins are transported to the areas where they are needed. Researchers are working to determine how mutations in the SEC23B gene lead to the signs and symptoms of CDA type II. Analyses of CDA II erythrocyte membranes showed that the band 3 glycoprotein is underglycosylated. An aberrant glycosylation pattern is seen in the polylactosamine carbohydrates which are normally attached to the band 3 and band 4.5 glycoproteins. The polylactosamines are, however, accumulated ...
TY - JOUR. T1 - Congenital dyserythropoietic anaemia type II (CDA‐II). T2 - chromosomal banding studies and adherent cell effects on erythroid colony (CFU‐E) and burst (BFU‐E) formation. AU - Roodman, G. D.. AU - Clare, C. N.. AU - Mills, G.. PY - 1982/3. Y1 - 1982/3. N2 - Bone marrow CFU‐E and BFU‐E from a patient with CDA‐II formed erythroid colonies and bursts which contained multinucleated erythroblasts in vitro. Adherent cell depletion of the patients marrow increased CFU‐E derived colonies six‐fold (98 ± 17 v. 640 ± 15 per 105 marrow cells plated) and co‐culture of CDA‐II marrow adherent cells with CDA‐II adherent cell depleted marrow significantly suppressed erythroid colony formation. Similar adherent cell suppression of the patients BFU‐E also occurred. Adherent cell depletion of normal marrow did not increase CFU‐E derived colony formation (488 ± 63 v. 495 ± 108) and decreased BFU‐E derived burst formation. Addition of normal adherent cells to normal ...
TY - JOUR. T1 - Congenital dyserythropoietic anemia type II in human patients is not due to mutations in the erythroid anion exchanger 1 [8]. AU - Perrotta, Silverio. AU - Luzzatto, Lucio. AU - Carella, Massimo. AU - Iolascon, Achille. PY - 2003/10/1. Y1 - 2003/10/1. UR - http://www.scopus.com/inward/record.url?scp=0141705291&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0141705291&partnerID=8YFLogxK. U2 - 10.1182/blood-2003-07-2389. DO - 10.1182/blood-2003-07-2389. M3 - Article. C2 - 14504075. AN - SCOPUS:0141705291. VL - 102. SP - 2704. EP - 2705. JO - Blood. JF - Blood. SN - 0006-4971. IS - 7. ER - ...
The congenital dyserythropoietic anemias are a heterogeneous group of rare disorders primarily affecting erythropoiesis with characteristic morphological abnormalities and a block in erythroid maturation. Mutations in the CDAN1 gene, which encodes Codanin-1, underlie the majority of congenital dyserythropoietic anemia type I cases. However, no likely pathogenic CDAN1 mutation has been detected in approximately 20% of cases, suggesting the presence of at least one other locus. We used whole genome sequencing and segregation analysis to identify a homozygous T to A transversion (c.533T|A), predicted to lead to a p.L178Q missense substitution in C15ORF41, a gene of unknown function, in a consanguineous pedigree of Middle-Eastern origin. Sequencing C15ORF41 in other CDAN1 mutation-negative congenital dyserythropoietic anemia type I pedigrees identified a homozygous transition (c.281A|G), predicted to lead to a p.Y94C substitution, in two further pedigrees of SouthEast Asian origin. The haplotype surrounding
The non-spherocytic hemolytic anemias comprise a seemingly diverse group of diseases intrinsic to the red cell when they are contrasted with the better known congenital hemolytic anemias, such as hereditary spherocytosis. Knowledge of their inheritance, course, and pathogenesis is incomplete. Since initially defined by Dacie (1) in 1953 as atypical congenital hemolytic anemia the general characteristics of this syndrome have been outlined (2, 3): [1] although hereditary, the anemia affects siblings rather than parents within a family; [2] the erythrocytes tend to be macrocytic, and spherocytes are absent; [3] the osmotic fragility of fresh native blood is not increased; [4] ...
BACKGROUND AND OBJECTIVES: Congenital dyserythropoietic anemia type III (CDA-III) is a group of very rare disorders characterized by similar bone marrow morphology. The clinical picture is characterized by hemolytic anemia and dramatic bone marrow changes dominated by active erythropoiesis with big multinucleated erythroblasts. The aim of this review is to describe the clinical manifestations, laboratory findings, and management CDA-III. EVIDENCE AND INFORMATION SOURCES: The present review critically examines relevant articles and abstracts published in journals covered by the Science Citation Index and Medline. The authors have performed several studies on CDA-III. STATE OF ART AND PERSPECTIVES: The clinical and laboratory manifestations of CDA-III indicate that the gene responsible for it, which has been mapped to chromosome 15q22, is expressed not only in erythroblasts during mitosis but also in B-cells, and in cells of the retina. Preliminary results indicate genetic and phenotypic ...
Congenital dyserythropoietic anemia (CDA) is a rare blood disorder, similar to the thalassemias. CDA is one of many types of anemia, characterized by ineffective erythropoiesis, and resulting from a decrease in the number of red blood cells (RBCs) in the body and a less than normal quantity of hemoglobin in the blood. The symptoms and signs of congenital dyserythropoietic anemia are consistent with: Tiredness (fatigue) Weakness Pale skin CDA may be transmitted by both parents autosomal recessively or dominantly and has four different subtypes, CDA Type I, CDA Type II, CDA Type III, and CDA Type IV . CDA type II (CDA II) is the most frequent type of congenital dyserythropoietic anemias. More than 300 cases have been described, but with the exception of a report by the International CDA II Registry, these reports include only small numbers of cases and no data on the lifetime evolution of the disease. The diagnosis of congenital dyserythropoietic anemia can be done via sequence analysis of the ...
Hereditary Spherocytosis: A familial congenital hemolytic anemia characterized by numerous abnormally shaped erythrocytes which are generally spheroidal. The erythrocytes have increased osmotic fragility and are abnormally permeable to sodium ions.
Congenital dyserythropoietic anemia (CDA) is a rare group of red blood cell disorders characterized by ineffective erythropoiesis and increased iron absorption. To determine whether growth differentation factor 15 (GDF15) hyper-expression is associated with the ineffective erythropoiesis and iron-loading complications of CDA type I (CDA I), GDF15 levels and other markers of erythropoiesis and iron overload were studied in blood from 17 CDA I patients. Significantly higher levels of GDF15 were detected among the CDA I patients (10 239 +/- 3049 pg/mL) compared with healthy volunteers (269 +/- 238 pg/mL). In addition, GDF15 correlated significantly with several erythropoietic and iron parameters including Hepcidin-25, Ferritin, and Hepcidin-25/Ferritin ratios. These novel results suggest that CDA I patients express very high levels of serum GDF15, and that GDF15 contributes to the inappropriate suppression of hepcidin with subsequent secondary hemochromatosis ...
TY - JOUR. T1 - Ultrastructural, cell culture and karyotype study of bone marrow in a patient with congenital dyserythropoietic anaemia (CDA)-type III presenting with recurrent still-births. AU - Ghosh, Kanjaksha. AU - Yavagal, Dilip. AU - Phillips, Callista. AU - Jijina, Farah. AU - Pathare, A. V.. AU - Kerketta, Lily. AU - Iyer, Y. S.. AU - Nair, C. N.. AU - Shinde, S.. AU - Mohanty, Dipika. PY - 1998. Y1 - 1998. N2 - A 28 year old female patient presented with refractory anaemia since childhood and recurrent still-births at 28-30 weeks of gestation. One still-born child was hydropic at birth. Bone marrow showed characteristic morphological changes of congenital dyserythropoietic anaemia (CDA)-Type III. Electron microscopy showed disruption of the nuclear membrane, spongy appearance of nuclei, stacks of microtubules in intermediate normoblasts and myelin figures in erythroid cells. In vitro culture and karyotype data from the bone marrow of the patient is presented. Recurrent still-births in ...
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Looking for online definition of stomatocytosis in the Medical Dictionary? stomatocytosis explanation free. What is stomatocytosis? Meaning of stomatocytosis medical term. What does stomatocytosis mean?
The clinical and haematological features of an unusual case of congenital dyserythropoietic anaemia are described. There was a pronounced haemolytic component to the anaemia, with a mean cell life of five days, and a remarkable response to splenectomy. Measurement of the incorporation of 15N glycine into the haem of circulating red cells and into bilirubin showed that haem turnover due to ineffective erythropoiesis was increased 45 times compared with a control group (11.63 mg/kg/day, NR = 0.26 + 0-10) and represented 51% of total erythroid haem turnover.. ...
Nail Hypoplasia, Polychromasia in Peripheral Blood Smear, Sinus Opacification Symptom Checker: Possible causes include Congenital Dyserythropoietic Anemia Type 1, Chronic Sinusitis, Congenital Dyserythropoietic Anemia. Check the full list of possible causes and conditions now! Talk to our Chatbot to narrow down your search.
The sickle cell anemia (SCA) is a hereditary hemolytic anemia. The polymerization of hemoglobin S (HbS) in the deoxygenated state in sickle cell disease (SCD) is the watershed event leading to vase- occlusion, factors that retard the transit time of sickle erythrocytes in the microcirculation and the cell s adhesive properties. The change in shape is responsible for the enhancing of adhesion in endothelial cells and vase occlusion impeding the blood flux to tissues (1) .The vascular occlusion is the result of a fall in oxygen tension in cells presenting a major density (2). The researches in electronic microscopy had been shown that the irreversible sickle cells does not have almost anything of polymerized hemoglobin and so still retains the sickle shape. The sickle shape occurs because the protein fixation in membrane cytoskeleton and they must not be responsible for the irreversibility shape of sickle cell. (3). these processes are dependent of sickle hemoglobin concentration. Thus, the ...
Knowledge of RBC membrane structure is important because defects in its structure underlie multiple IHAs [16]. The human RBC membrane consists of three basic components: a lipid bilayer, transmembrane linker proteins, and a two-dimensional spectrin-based cytoskeleton network [171819]. Connections of the two layers depend on different linker proteins with binding sites, respectively, for the cytoplasmic domains of the integral membrane proteins (band 3 and glycophorin C) embedded in the lipid bilayer and specific regions of spectrin proteins in the cytoskeleton (Fig. 1). RBC membranopathies are the result of qualitative abnormalities or quantitative deficiencies of the RBC cytoskeletal proteins and can be divided into those resulting from structural protein loss including HS, hereditary elliptocytosis (HE) and hereditary ovalocytosis and membrane transport dysfunction (hereditary stomatocytosis) (Fig. 2) [1620]. Defects that interrupt the vertical structure (spectrin-actin interaction) underlie ...
cdna: chromosome:VEGA66:2:120716522:120731518:-1 gene:OTTMUSG00000015621 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Cdan1 description:congenital dyserythropoietic anemia type I (human ...
Dyserythropoietic anemia is a condition that influences platelets and principally observed in males. Dyserythropoietic anemia is one of numerous sorts of i..
Ion channels are transmembrane proteins that allow ions to move in or out of cells, and they are vital to a range of biological processes. They can be opened and closed in a number of ways: for example, some are opened by voltage, while others respond to the binding of ligands. Piezo1 and Piezo2 are mechanosensitive ion channels: in other words, they open in response to mechanical stimulation, such as stretching or shear stress (Coste et al., 2010, 2012).. Mutations in the gene Piezo1 have been linked to a blood disease called xerocytosis that leads to hemolytic anemia (Albuisson et al., 2013; Bae et al., 2013; Coste et al., 2013; Zarychanski et al., 2013). It is known that these mutations reduce the ability of the Piezo1 ion channel to close, and this leads to red blood cells shrinking as a result of dehydration. However, the details of this process are not fully understood. Now, in a pair of papers in eLife, Ardem Patapoutian, Michael Bandell and colleagues at the Scripps Research Institute, ...
Learn about the causes, symptoms, diagnosis & treatment of Anemias Caused by Hemolysis from the Professional Version of the Merck Manuals.
PIs piezo drivers are available as benchtop or rackmount solutions, and as OEM modules also with separate power supply for minimized size.
Click on a [studies] link to search within your current results for studies in that region. Use the back button to return to this list and try another region ...
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