Background: On-therapy impedance-pH monitoring in proton pump inhibitor (PPI)-refractory gastroesophageal reflux disease (GERD) yielded conflicting results. We aimed to assess the diagnostic value of postreflux swallow-induced peristaltic wave (PSPW) index and mean nocturnal baseline impedance (MNBI) in PPI-refractory heartburn. Methods: On-therapy impedance-pH tracings from 189 consecutive patients with PPI-refractory heartburn were blindly reviewed. Patients were subdivided into refractory reflux esophagitis (RRE), healed reflux esophagitis (HRE), non-erosive reflux disease (NERD), and functional heartburn (FH) according to endoscopic and conventional impedance-pH findings. The diagnostic accuracy of PSPW index and MNBI in separating NERD from FH was assessed with receiver-operating-characteristic (ROC) analysis. Objectively documented persistent reflux remission at 3-year follow-up in 53 patients who underwent laparoscopic fundoplication served to evaluate PSPW index and MNBI as independent ...
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Aim of this volume is to clarify the relationship between molecular structure and function of tight junction proteins, as well as their regulation and their role in diseases. Current research may form a basis for future diagnostic and therapeutic approaches to diseases which seem to have not much in common but are characterized by defects of organ barriers, like Crohns disease, renal hypertension, inner ear deafness, and cancerous diseases. Topics include the functions of distinct tight junction proteins as barrier or channel formers for solutes and water, characteristics of the tight junction in inflammatory bowel diseases, posttranslational modifications of tight junction proteins, the relation between renal tight junction proteins and blood pressure control, and the molecular structure of claudin-claudin interactions NOTE: Annals volumes are available for sale as individual books or as a journal. For information on institutional journal subscriptions, please visit www.blackwellpublishing.com/nyas.
Mouse monoclonal ZO1 tight junction protein antibody [mAbcam 61357] validated for WB, IP, Flow Cyt and tested in Human. Referenced in 2 publications and 5…
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Tight junctions between epithelial and endothelial cells form selective barriers and paracellular channels and regulate paracellular transport of solutes, immune cells, and drugs. More specifically, tight junctions consist of proteins that laterally interconnect neighboring cells of epithelia and endothelia. Certain proteins seal the tight junction, so that a nearly impermeable barrier develops, whereas others form channels that allow for permeation between the cells. Recent investigations have focused on tight junction proteins, belonging to the claudin family (claudins-1 to -27 in humans) and the newly defined group of TAMP (three proteins: occludin, Marvel-D2, and tricellulin). Barriers and Channels Formed by Tight Junction Proteins I showcases work in this area clustered around three major themes: the molecular properties of tight junctions, for example, the role of the claudin family of proteins and the formation of ion and charge-selective channels; the regulation of tight junction
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The relationship between the molecular structure and function of tight junction proteins, as well as their regulation and their role in disease, is discussed.
Background The mind endothelium is a key component of the blood brain barrier which is compromised following ischemia allowing infiltration of damaging immune cells and other inflammatory molecules into the brain. that IVIg prevented the down-regulation of tight junction proteins claudin 5 and occludin and the decline in anti-apoptotic proteins Bcl-2 and Bcl-XL caused by […]. ...
The tight junction (TJ) is a dynamic structure that is controlled, in part, by the activity of the cytoskeleton. It has become abundantly clear that, in the presence of Ca2+, assembly of the TJ is the result of cellular interactions that trigger a complex cascade of biochemical events that ultimatel …
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Increased BSCB permeability extends throughout the spinal cord. A: left panel, representative spinal cord from naïve rats, rats 24 hours post C-fiber stimulati
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Impaired blood-brain barrier function represents a significant component of hypoxic-ischemic brain injury in the perinatal period. Banks, W. A., Stonestreet, B. S. AntiCIL-6 neutralizing antibody modulates blood-brain barrier function in the ovine fetus. mAb attenuate ischemia-reperfusionCrelated increases in BBB permeability in sheep fetuses (16). However, the role of IL-6 after injury in the immature brain has been studied much less extensively than those of IL-1and TNF-in the immature brain. We recently generated pharmacologic quantities of a highly selective, ovine-specific antiCIL-6 mAb and antiCIL-1mAb. The neutralizing abilities of these mAbs have previously been confirmed in ovine splenic mononuclear cell cultures (35). Moreover, we recently demonstrated that infusions of an antiCIL-1mAb result in the uptake of the antiCIL-1mAb into the brain and attenuate ischemia-reperfusionCrelated increases in BBB permeability in ovine fetal brain using the preclinical translational fetal sheep model ...
TY - JOUR. T1 - Chronic inflammatory pain leads to increased blood-brain barrier permeability and tight junction protein alterations. AU - Brooks, Tracy A.. AU - Hawkins, Brian T.. AU - Huber, Jason D.. AU - Egleton, Richard D.. AU - Davis, Thomas P. PY - 2005/8. Y1 - 2005/8. N2 - The blood-brain barrier (BBB) maintains brain homeostasis by limiting entry of substances to the central nervous system through interaction of transmembrane and intracellular proteins that make up endothelial cell tight junctions (TJs). Recently it was shown that the BBB can be modulated by disease pathologies including inflammatory pain. This study examined the effects of chronic inflammatory pain on the functional and molecular integrity of the BBB. Inflammatory pain was induced by injection of complete Freunds adjuvant (CFA) into the right plantar hindpaw in female Sprague-Dawley rats under halothane anesthesia; control animals were injected with saline. Edema and hyperalgesia were assessed by plethysmography and ...
Identify an antibody against an adhesion junction protein that is commercially available. Add a link to the original data sheet page and identify the type of adhesion junction. Include the following information: type of antibody (polyclonal, monoclonal), species raised in, species reacts against, types of application uses, and if available any reference using that antibody. Tight Junction Protein 1 Antibody Original Data Sheer for Tight Junction Protein 1 Antibody Type of adhesion junction: human zona occludens 1, specifically ZO-1 alpha-minus found both in endothelial cells and the highly specialized epithelial junctions of renal glomeruli and Sertoli cells of the seminiferous tubules. Type of antibody: Polyclonal Species raised in: Guinea Pig Species reactivity: Human, Mouse, Rat, and Canine Types of application uses: Immunohistology, immunofluorescence and Western blotting References that uses this antibody: 1. ,pubmed,22314269,/pubmed,[3] 2. ,pubmed,22162948,/pubmed,[4] ...
Identify an antibody against an adhesion junction protein that is commercially available. Add a link to the original data sheet page and identify the type of adhesion junction. Include the following information: type of antibody (polyclonal, monoclonal), species raised in, species reacts against, types of application uses, and if available any reference using that antibody. Tight Junction Protein 1 Antibody Original Data Sheer for Tight Junction Protein 1 Antibody Type of adhesion junction: human zona occludens 1, specifically ZO-1 alpha-minus found both in endothelial cells and the highly specialized epithelial junctions of renal glomeruli and Sertoli cells of the seminiferous tubules. Type of antibody: Polyclonal Species raised in: Guinea Pig Species reactivity: Human, Mouse, Rat, and Canine Types of application uses: Immunohistology, immunofluorescence and Western blotting References that uses this antibody: 1. ,pubmed,22314269,/pubmed,[3] 2. ,pubmed,22162948,/pubmed,[4] ...
The Hippo pathway, by tightly controlling the phosphorylation state and activity of the transcription cofactors YAP and TAZ is essential during development and tissue homeostasis whereas its deregulation may lead to cancer. Recent studies have linked the apicobasal polarity machinery in epithelial cells to components of the Hippo pathway and YAP and TAZ themselves. However the molecular mechanism by which the junctional pool of YAP proteins is released and activated in epithelial cells remains unknown. Here we report that the tumour suppressor ASPP2 forms an apical-lateral polarity complex at the level of tight junctions in polarised epithelial cells, acting as a scaffold for protein phosphatase 1 (PP1) and junctional YAP via dedicated binding domains. ASPP2 thereby directly induces the dephosphorylation and activation of junctional YAP. Collectively, this study unearths a novel mechanistic paradigm revealing the critical role of the apical-lateral polarity complex in activating this localised pool of
The TJP2 protein (Tight Junction Protein 2, sometimes called ZO2) plays a role in "tight junctions". Tight junctions are areas where the membranes of two adjacent cells join to form a barrier. The barrier controls what molecules are able to pass between cells. Such junctions are important throughout the body, and TJP2 is not specific to the liver. A mild form of liver disease associated with mutations in the TPJ 2 gene was previously called familial hypercholanaemia (which means high bile salts in blood). Only a small number of patients with PFIC caused by TJP2 mutation have been studied so far, so it is not yet understood of what manifestations, other than liver disease and its consequences that TJP2 deficiency patients may have.. ...
Epithelial layers are integral for many physiological processes and are maintained by intercellular adhesive structures. During disease, these structures can disassemble, leading to breakdown of epithelia. TJs (tight junctions) are one type of intercellular adhesion. Loss of TJs has been linked to the pathogenesis of many diseases. The present review focuses on the role of vesicle trafficking in regulation of TJs, in particular trafficking of the TJ protein occludin. We examine how endocytosis and endosomal recycling modulate occludin localization under steady-state conditions and during stimulated TJ disassembly. ...
Mucosal surfaces are lined by epithelial cells and provide an important barrier to the flux of antigens from the outside. This barrier is provided at a number of levels, including epithelial junctional complexes, mucus production, and mucosa-derived antimicrobials. Tissue metabolism is central to the maintenance of homeostasis in the mucosa. In the intestine, for example, baseline pO2 levels are uniquely low due to counter-current blood flow and the presence of large numbers of bacteria. As such, hypoxia and HIF signaling predominates normal intestinal metabolism and barrier regulation during both homeostasis and active inflammation. Contributing factors that elicit important adaptive responses within the mucosa include the transcriptional regulation of tight junction proteins, metabolic regulation of barrier components, and changes in autophagic flux. Here, we review recent literature around the topic of hypoxia and barrier function in health and during disease.. ...
Health Categories: Gluten Sensitivity Probiotic/Microbiome Clinical Dose of Quercetin, Bioferrin, Turmeric and L-Alynyl Glutamine in an herbalomic support blend. Lab studies have demonstrated the ability of Quercetin to support the intestinal mucosa by up-regulating the tight junction protein claudin and down-regulatin
1. What is the distance between the points (1, 4) and (4, 8)? I said Distance = 5 2. Find the slope between (1, 4) and (4, 8) I said 4/3 3. Are the expressions (4x+4)/4 and x+1 equivalent? I said Yes 4. Simplify (x+y)2 x2 + 2xy + y2 5. Is (x - y )2 = x2 - y2? No. It is ... ...
Our results uncover a novel function for cytoplasmic YAP1. YAP1 recruits c-Abl to protect AMOTL1 against Nedd4.2-mediated degradation. Thus, YAP1, excluded from the nucleus, contributes to the maintenance of tight junctions.
Characterization of the tight junction is proceeding rapidly and has stimulated advances in the fields of cell-cell interactions and epithelial cell biology. In addition to the list of proteins now found at the tight junction, we have learned that two previously characterized tight junction components, ZO-1 and ZO-2, are members of a larger protein family that appear to function in the organization of specific areas of the cell surface (11, 21, 23, 24, 27, 41, 44). Moreover, data suggest that some members of this family are involved in signal transduction and/or tumor suppression (1, 41, 46, 47), highlighting the importance of analyzing these molecules.. Here we present evidence of a novel member of the MAGUK family of proteins found at the tight junction. This 130-kD polypeptide, named ZO-3 because of homology to ZO-1 and ZO-2 (Figs. 5, Tables II and III) and localization at the tight junction (Figs. 7 and 8), contains 3 PDZ domains, an SH3 domain and a GUK region (Fig. 3). The arrangement of ...
Caco-2 monolayers grown on permeable filters for 21 days in bicameral Transwell chambers were incubated with control medium, medium containing cytomix (CM), a cocktail containing the pro-inflammatory cytokines, IL-1β (1 μg/ml), TNF (10 ng/ml) and IFN-γ (1000 U/ml), or medium containing CM and one of these other pharmacologic agents: ethyl pyruvate (EP; H2O2 scavenger; 10 mM): PJ34 (PARP inhibitor; 5 μM): 3-aminobenzamide (3-AB; PARP inhibition; 3 μM): FeTPPS (ONOO- decomposition catalyst; 50 μM): C-PTIO (NO• scavenger; 100 μM): PDTC (NF-κB inhibitor; 100 μM) or L-NIL (selective iNOS inhibitor; 20 μM). Permeability was expressed as the apical-to-basolateral clearance (nLcm-1 h-1) of fluorescein-labelled dextran (FD4) during the last 48 hours of incubation. Expression of occludin and ZO-1 were assessed by Western blot and immunohistochemistry. ...
Our research should stimulate renewed clinical interest in developing glucocorticoid therapies to treat blast-induced traumatic brain injury (bTBI) and other disorders of the central nervous system," Morrison says. His findings also hold important implications for military personnel exposed to blast injury. "We may be able to improve outcomes in brain-injured soldiers and civilians," he continues, "and reduce the length of their mandatory rest periods before returning to duty, making the difference between requiring only days rather than weeks or longer to recover.". This improvement could be a significant result, as there are currently no approved pharmaceutical therapies for traumatic brain injury (TBI), and recently completed clinical trials have not demonstrated any benefit of other tested neuro-protective interventions. For patients with head injuries (non-blast related) and brain edema, doctors have been prescribing glucocorticoids, a class of steroid hormones, as standard treatment for ...
The C\terminal fragment of enterotoxin (C\CPE) modulates the tight junction protein claudin and disturbs the tight junctional barrier. epithelial cells (HPDEs) had been treated with C\CPE 194 and C\CPE meters19. In well\differentiated cells of the pancreatic malignancy cell collection HPAC, C\CPE 194 and C\CPE meters19 interrupted both the hurdle and fencing features without adjustments in manifestation of claudin\1 and \4, collectively with an boost of MAPK phosphorylation. C\CPE 194, but not really C\CPE meters19, improved the cytotoxicity of the anticancer brokers gemcitabine and H\1. In differentiated pancreatic malignancy cell collection PANC\1 badly, C\CPE 194, but not really C\CPE meters19, reduced claudin\4 phrase and improved MAPK activity and the cytotoxicity of the anticancer agencies. In regular HPDEs, C\CPE 194 and C\CPE meters19 reduced claudin\4 phrase and improved the MAPK activity, whereas they do not really influence the cytotoxicity of the anticancer agencies. Our results ...
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All of us in the business talk about the blood-brain barrier, but. . .no, Im not going to end this sentence with . . .none of us do anything about it,
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Tamou, coded for by polychaetoid, a Drosophila cell-cell junction-associated protein, is homologous to mammalian ZO-1, a member of the membrane-associated guanylate kinase homolog family. It is suggested that TAM is in an emc activating pathway. Mutation in tam gives a phenotype resembling mutation in emc. Mammalian ZO-1 can bind directly to the cytoskeletal element alpha-spectrin, and also binds occludin, an integral membrane protein at the tight junction. It is proposed that ZO-1 plays a role in the structural linkages between the tight junction and cytoskeletal networks. ZO-1 also colocalizes with cadherins in nonepithelial cells lacking tight junctions. Mutation in tam reduces the transcription of emc and causes enlargement of proneural clusters resulting in emergence of supernumerary precursor cells, and consequently in extra mechanosensory organs (Takahisa, 1996). Irregular facets (If) is a dominant mutation of Drosophila that results in small eyes with fused ommatidia. Previous results ...
TY - JOUR. T1 - Adherence of Yersinia enterocolitica to Mammalian Epithelial Cell Lines. AU - Okamoto, Keinosuke. AU - Inoue, Takashi. AU - Ichikawa, Hidetaka. AU - Kawamoto, Yasuko. AU - Hara, Susumu. AU - Miyama, Akio. PY - 1980. Y1 - 1980. N2 - Yersinia enterocolitica RIMD 2501003 grown at 25 C avidly adhered to various kinds of cultured epithelial cell lines (HeLa, FL, Y-1 adrenal, human intestine, human conjunctiva) but the bacteria grown at 37 C did not adhere. This phenomenon paralleled the temperature-dependent motility of the bacteria. To clarify the adherence mechanism, we obtained two kinds of mutants, an im-mobile mutant and a nonadherent mutant, by treatment with N-methyl-N′-nitro-N-nitrosoguanidine. The immobile mutant did not move on soft agar but retained the capacity to adhere to cultured epithelial cells when grown at 25 C. The nonadherent mutant did not adhere to cultured epithelial cells but retained the ability to move on soft agar when grown at 25 C. When the bacteria ...
In mammalian epithelial cells, the most apical components of the lateral junctional complex are TJs that serve as intercellular barriers to regulate paracellular permeability and function as intramembranous fences to maintain the polarization of the apical and basolateral membrane domains ( Mitic and Anderson, 1998; Cereijido et al., 1998). A growing number of TJ-associated peripheral or integral proteins have been identified, and the characterized properties of these proteins provide a molecular basis for TJ formation and function. However, at present it is not fully understood how the formation of this complicated junctional structure is orchestrated in terms of the dynamic process.. We have previously identified ASIP, the mammalian homolog of C. elegans polarity protein PAR-3, as an epithelial TJ-associated peripheral protein ( Izumi et al., 1998); however, the physiological functions of mammalian ASIP/PAR-3 remain to be clarified. In this study, we provide two lines of evidence suggesting ...
Diabetes mellitus (DM) is a high risk factor for stroke and leads to more severe vascular and white-matter injury than stroke in non-DM. We tested the neurorestorative effects of delayed human umbilical cord blood cell (HUCBC) treatment of stroke in type-2 diabetes (T2DM). db/db-T2DM and db/+-non-DM mice were subjected to distal middle cerebral artery occlusion (dMCAo) and were treated 3 days after dMCAo with: (a) non-DM + Phosphate buffered saline (PBS); (b) T2DM + PBS; (c) T2DM + naïve-HUCBC; (d) T2DM + miR-126(-/-) HUCBC. Functional evaluation, vascular and white-matter changes, neuroinflammation, and miR-126 effects were measured in vivo and in vitro. T2DM mice exhibited significantly decreased serum and brain tissue miR-126 expression compared with non-DM mice. T2DM + HUCBC mice exhibited increased miR-126 expression, increased tight junction protein expression, axon/myelin, vascular density, and M2-macrophage polarization. However, decreased blood-brain barrier leakage, brain hemorrhage, and miR
Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), ...
Cingulin is specifically localized at tight junctions in epithelial cells, unlike ZO-1, which is also detected at adherens-type junctions in non-epithelial cells ... development, cingulin is detected at a cortical localization, and then accumulates at apical junctions, unlike ZO-1 and other junctional proteins, that are targeted to the new regions ... Cingulin interacts with ZO-1 and several other tight junction proteins, in addition to interacting with actin and myosin ...
Barclay Morrison III, associate professor of biomedical engineering at Columbia Engineering, has led the first study to determine underlying biological mechanisms that promote functional recovery of the blood-brain barrier (BBB) after blast injury.
Occludin is an integral membrane protein, encoded by the OCLN gene, that is located at tight junctions. Tight junctions act as a physical barrier to prevent solutes and water from passing freely through the paracellular space. Occludin is also known as BLCPMG. It is known to interact with several cytoplasmic proteins via its C terminus, while its extracellular loops are thought to be involved in the regulation of paracellular permeability and cell adhesion. When occludin is expressed in cells that lack tight junctions, it is able to induce cell adhesion. Mutations in the OCLN gene are associated with an autosomal recessive neurologic disorder known as band-like calcification with simplified gyration and polymicrogyria (BLC-PMG).. ...
Occludin is an integral membrane protein, encoded by the OCLN gene, that is located at tight junctions. Tight junctions act as a physical barrier to prevent solutes and water from passing freely through the paracellular space. Occludin is also known as BLCPMG. It is known to interact with several cytoplasmic proteins via its C terminus, while its extracellular loops are thought to be involved in the regulation of paracellular permeability and cell adhesion. When occludin is expressed in cells that lack tight junctions, it is able to induce cell adhesion. Mutations in the OCLN gene are associated with an autosomal recessive neurologic disorder known as band-like calcification with simplified gyration and polymicrogyria (BLC-PMG).. ...
When DArcy Wentworth Thompsons On Growth and Form was published 100 years ago, it raised the question of how biological forms arise during development and across evolution. In light of the advances in molecular and cellular biology since then, a succinct modern view of the question states: how do genes encode geometry? Our new special issue is packed with articles that use mathematical and physical approaches to gain insights into cell and tissue patterning, morphogenesis and dynamics, and that provide a physical framework to capture these processes operating across scales.. Read the Editorial by guest editors Thomas Lecuit and L. Mahadevan, as they provide a perspective on the influence of DArcy Thompsons work and an overview of the articles in this issue.. ...