Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cellular Structures”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,603 records · Page 89Linked to original sources

Compared with crystalloid, colloid therapy slows progression of extrapulmonary tissue injury in septic sheep.

We tested the hypothesis that the type of fluid infused to chronically maintain intravascular volumes would modify both microvascular integrity and cellular structure in extrapulmonary organs in hyperdynamic sepsis. After cecal ligation and perforation, awake sheep were treated for 48 h with 10% pentastarch (n = 9), 10% pentafraction (Du Pont Critical Care; n = 8), or Ringer lactate (n = 8) titrated to maintain a constant left atrial pressure. After 48 h of fluid therapy, biopsy samples were taken from the left ventricle and gastrocnemius for electron microscopy. At this time, all groups demonstrated a similar hyperdynamic circulatory response, increased systemic O2 utilization and organ blood flows, measured by radioactive microsphere injection. However, greater capillary luminal areas with less endothelial swelling and less parenchymal injury were found in septic sheep treated with pentastarch vs. Ringer lactate infusion in both muscle types. Pentafraction showed few benefits in study end points over pentastarch. Thus, we conclude that chronic intravascular volume resuscitation of hyperdynamic sepsis with pentastarch ameliorated the progression of both microvascular and parenchymal injury. These findings indicate that microvascular surface area for tissue O2 exchange in sepsis may be better preserved with chronically infused colloid, resulting in less parenchymal injury.

Animals↗

In vivo calcium imaging of circuit activity in cerebellar cortex.

In vivo two-photon calcium imaging provides the opportunity to monitor activity in multiple components of neural circuitry at once. Here we report the use of bulk-loading of fluorescent calcium indicators to record from axons, dendrites, and neuronal cell bodies in cerebellar cortex in vivo. In cerebellar folium crus IIa of anesthetized rats, we imaged the labeled molecular layer and identified all major cellular structures: Purkinje cells, interneurons, parallel fibers, and Bergmann glia. Using extracellular stimuli we evoked calcium transients corresponding to parallel fiber beam activity. This beam activity triggered prolonged calcium transients in interneurons, consistent with in vitro evidence for synaptic activation of N-methyl-d-aspartate receptors via glutamate spillover. We also observed spontaneous calcium transients in Purkinje cell dendrites that were identified as climbing-fiber-evoked calcium spikes by their size, time course, and sensitivity to AMPA receptor antagonist. Two-photon calcium imaging of bulk-loaded cerebellar cortex is thus well suited to optically monitor synaptic processing in the intact cerebellum.

Animals↗

Physiological properties of the normal lens.

The lens is an avascular organ suspended between the aqueous and vitreous humors of the eye. The cellular structure is symmetric about an axis passing through its anterior and posterior poles but asymmetric about a plane passing through its equator. Because of its asymmetric structure, the lens has historically been assumed to perform transport between the aqueous and vitreous humors. Indeed, when anterior and posterior surfaces were isolated in an Ussing chamber, a translens current was measured. However, in the eye, the two surfaces are not isolated. The vibrating probe technique showed the current densities at the surface of a free-standing lens were surprisingly large, about an order of magnitude greater than measured in an Ussing chamber, and were not directed across the lens. Rather, they were inward in the region of either anterior or posterior pole and outward at the equator. This circulating current is the most dramatic physiological property of a normal lens. We believe it is essential to maintain clarity; hence, this review focuses on factors likely to drive and direct it. We review properties and spatial distribution of lens Na+/K+ pumps, ion channels, and gap junctions. Based on these data, we propose a model in which the difference in electromotive potential of surface versus interior cell membranes drives the current, whereas the distribution of gap junctions directs the current in the observed pattern. Although this model is clearly too simple, it appears to quantitatively predict observed currents. However, the model also predicts fluid will move in the same pattern as ionic current. We therefore speculate that the physiological role of the current is to create an internal circulatory system for the avascular lens.

Animals↗

Calcitonin gene-related peptide and substance P regulate the intestinal radiation response.

PURPOSE: Intestinal toxicity is important in the therapeutic use of radiation as well as in nontherapeutic radiation exposure scenarios. Enteric sensory nerves are critical for mucosal homeostasis and for an appropriate response to injury. This study assessed the role of the two major neuropeptides released by sensory nerves, calcitonin gene-related peptide (CGRP) and substance P, in the intestinal radiation response. EXPERIMENTAL DESIGN: Male rats received full-length CGRP, CGRP antagonist (CGRP(8-37)), a modified substance P peptide (GR73632), a small-molecule substance P receptor antagonist (neurokinin-1 receptor antagonist, SR140333), or vehicle for 2 weeks after localized X irradiation of a 4-cm loop of small bowel. Structural, cellular, and molecular aspects of the intestinal radiation response were assessed. RESULTS: Intestinal CGRP and substance P transcript levels increased after irradiation. Multivariate analysis showed that CGRP and SR140333 ameliorated and CGRP(8-37) and GR73632 exacerbated intestinal radiation injury. Univariate analysis revealed increased radiation injury score, bowel wall thickening, and collagen III deposition after treatment with CGRP(8-37), whereas SR140333 ameliorated radiation injury score, loss of mucosal surface area, collagen III deposition, and mucosal inflammation. CONCLUSIONS: The two major neuropeptides released by sensory neurons, CGRP and substance P, are overexpressed after irradiation and have opposing effects during development of intestinal radiation injury. Systematic studies to assess CGRP agonists and/or neurokinin-1 receptor blockers as protectors against intestinal toxicity during radiation therapy and after nontherapeutic radiation exposure are warranted.

Adenosine↗

Cisplatin preferentially binds mitochondrial DNA and voltage-dependent anion channel protein in the mitochondrial membrane of head and neck squamous cell carcinoma: possible role in apoptosis.

PURPOSE: Cisplatin adducts to nuclear DNA (nDNA) are felt to be the molecular lesions that trigger apoptosis, but the mechanism linking nDNA adduct formation and cell death is unclear. Some literature in the last decade has suggested a possible direct effect of cisplatin on mitochondria independent of nDNA interaction. In this study, we define separately the sequelae of cisplatin interactions with nDNA and with mitochondria in head and neck squamous cell carcinoma (HNSCC) cell lines. EXPERIMENTAL DESIGN: Cisplatin binding to mitochondrial DNA (mtDNA) and proteins was analyzed by atomic absorption spectroscopy and other methods. RESULTS: Following 1 hour of exposure to cisplatin, platinum adducts to mtDNA were 300- to 500-fold more abundant than adducts to nDNA; these differences were not due to differences in rates of adduct repair. Whereas HNSCC cell cytoplasts free of nDNA retained the same dose-dependent cisplatin sensitivity as parental cells, HNSCC rho(0) cells free of mtDNA were 4- to 5-fold more resistant to cisplatin than parental cells. Isolated mitochondria released cytochrome c within minutes of exposure to cisplatin, and ultrastructural analysis of intact HNSCC cells by electron microscopy showed marked mitochondrial disruption after 4 hours of cisplatin treatment, whereas the nucleus and other cellular structures remain intact. The very prompt release of cytochrome c from isolated mitochondria implies that apoptosis does not require alteration in mitochondrial gene transcription. Further, cisplatin binds preferentially to mitochondrial membrane proteins, particularly the voltage-dependent anion channel. CONCLUSIONS: Cisplatin binding to nDNA is not necessary for induction of apoptosis in HNSCC, which can result from direct action of cisplatin on mitochondria.

Antineoplastic Agents↗

Molecular cloning and characterization of hazel pollen protein (70 kD) as a luminal binding protein (BiP): a novel cross-reactive plant allergen.

BACKGROUND: Tree pollen contains many allergens showing cross-reactivity to proteins from pollen, seeds, and fruits of different plant species. Amongst Fagales, responsible for several allergenic responses, hazel provides the best material to study pollen as well as food allergens in one species. The aim of this study was to identify and characterize the physiological function of an allergen from hazel pollen and to determine possible cross-reactivity to proteins from hazelnut. METHODS: Monoclonal antibodies (mAbs) against hazel pollen crude extract were produced. On the basis of IgE binding, demonstrated by sera from patients allergic to hazel pollen, one mAb indicating the best correlation has been selected, and the putative allergen was purified by preparative gel electrophoresis. Isoforms were investigated by two-dimensional PAGE, and for molecular identification a hazel pollen cDNA library was constructed. In situ localization of the allergen during pollen development was performed by immunofluorescence labelling. RESULTS: Immunological staining of crude hazel pollen extract with specific IgE and mAb revealed a 70-kD protein. Immunoblot studies with mAb showed cross-reactive proteins of 70-72 kD in different plant tissues and species. After protein purification, the IgE-binding reactivity of the allergen has been reconfirmed, and two isoforms were detected. Molecular cloning identified the allergen as a luminal binding protein (BiP) of the Hsp70 family with 88-92% sequence identity in various plants. Further immunocytological studies indicated involvement of BiP during pollen development. CONCLUSIONS: Chaperons like BiP play an important role in protein synthesis and in the protection of cellular structures during stress-related processes. Because of their highly conserved protein sequences, we propose that such allergens could be responsible for at least a part of the allergenic cross-reactivity between proteins from different pollens and plant foods.

Allergens↗

Elucidation of cell secretion: pancreas led the way.

Secretion is a basic process in all cells and is required for several important functions such as neurotransmission, the secretion of digestive juices from the exocrine pancreas and the release of hormones from endocrine and neuroendocrine cells. Due to these important functions, the mechanism of cell secretion has been intensely investigated for over half a century. However, it is only in the last decade, with the discovery of a new cellular structure, the 'porosome' or 'fusion pore', and the elucidation of SNARE-induced membrane fusion, that has finally provided us with an understanding of cell secretion at the molecular level. The 'porosome', a supramolecular structure at the cell plasma membrane, was first discovered in the exocrine pancreas, and subsequently in endocrine/neuroendocrine cells and in neurons. The structure and dynamics of the 'porosome' in live cells at nanometer resolution and in real-time, its composition and functional reconstitution in lipid membrane, have all been determined. These findings have fundamentally changed our understanding of cell secretion and provide a clear understanding of this highly regulated process in cells.

Animals↗

Calcium in the brain under physiological and pathological conditions.

This paper reviews the role of calcium in the brain under physiological and pathological conditions. Calcium is a ubiquitous first and second messenger, and a regulator of metabolic pathways, serving the purpose of transforming external messages into the appropriate cellular metabolic responses. At least three voltage-sensitive calcium channels (L, T and N) are involved as well as agonist-operated calcium channels (AOCCs). The latter are the major contributors to postsynaptic calcium entry, the majority being gated by glutamate receptors. Intracellular release occurs from endoplasmatic reticulum and other sites (calcisomes). The calcium hypothesis of cell necrosis postulates that whenever free intracellular calcium concentrations become pathologically enhanced, calcium-activated reactions may become uncontrolled adversely altering cell functioning and disrupting cellular structures. Excessive calcium influx is now thought to occur primarily via AOCCs, more particularly those activated by glutamate.

Brain↗

Platelet-derived growth factor: a general review with emphasis on astrocytomas.

Growth factors acting in a paracrine or autocrine fashion are important in the development of normal cellular structures, and possibly in the development of neoplasia. For example, platelet-derived growth factor (PDGF) has been found in many normal tissues including the CNS, while minor changes in one of its forms (PDGF-B) converts it to the v-sis oncogene, capable of inducing sarcomas and astrocytomas in primates. PDGF is highly expressed in many human astrocytoma-derived cell lines, some of which also possess the PDGF-receptor(s), suggestive of an autocrine loop. Whether this finding is also present in the actual tumor, does it vary with tumor grade, what components of the tumor express PDGF and how does PDGF promote astrocytoma growth are some of the unanswered questions forming the basis of ongoing research efforts. This paper reviews the story of PDGF in a much oversimplified, however, hopefully understandable, fashion and presents the case of why this growth factor is of interest in understanding the biology of astrocytomas.

Animals↗

The anatomy of adipose tissue in captive Macaca monkeys and its implications for human biology.

In a sample of 31 sedentary, ad libitum-fed monkeys, most specimens had less than 5% adipose tissue by weight. Total fatness correlated closely with the number of adipocytes per kilogram lean body mass, but not at all with mean adipocyte volume, except in specimens below 5% fat. The total number of adipocytes per kilogram of lean body mass increased more than tenfold in the most obese specimens. These data suggest that, like humans but in contrast to laboratory rodents, adipocyte proliferation, not adipocyte enlargement, is the chief mechanism of adipose tissue expansion except in very lean monkeys. Adipose tissue was found in all the typical mammalian depots and in the superficial abdominal paunch, which enlarged disproportionately in obese specimens, forming an almost continuous layer over most of the body. Site-specific differences in the activities of some glycolytic enzymes were similar to those of other mammals. Adipocytes in the paunch depot showed biochemical properties in common with those in the groin depots. The distribution and cellularity of adipose tissue in normal humans were similar to those of exceptionally obese monkeys. Many of the interspecific and sex differences can be attributed to the much greater abundance of adipose tissue in humans, and may not be associated with hair reduction or aquatic habits. Some minor changes in the size or shape of certain adipose depots may have arisen recently under sexual selection. The relevance of laboratory rodents as animal models of human obesity is assessed from comparison of the cellular structure, anatomical distribution and enzyme profiles of adipose tissue in monkeys with those of human and other mammals.

Adipose Tissue↗

Induction of cell-rich and lipid-rich plaques in a transfilter coculture system with human vascular cells.

Cell-to-cell interactions are mainly involved in the control of the proliferation, migration, differentiation and function of different cell types in a wide range of tissues. In the arterial vessel wall, human arterial endothelial cells (haEC) and smooth muscle cells (haSMC) coexist in close contact with each other. In atherogenesis, haSMC can migrate from the media to the subintimal space to form fibromuscular and atheromatous plaques. In the present study, a transfilter coculture system is described, in which the interface between haSMC and confluent or proliferative haEC can be studied in detail. Cells were cocultured on the opposite sides of a porous filter which separates both cell types like the internal elastic lamina in vivo. In cocultures containing proliferative haEC, haSMC growth was significantly stimulated (33.4 +/- 5.7 cells/section, p < 0.05) compared to haSMC monocultures (22.9 +/- 2.5 cells/section) and cocultures containing confluent haEC (15.6 +/- 2.9 cells/section). If confluent haEC were injured mechanically, haSMC growth increased highly significantly (71.3 +/- 16.8 cells/section, p < 0.001). Thus, cell-rich proliferates containing 5-7 layers of haSMC embedded in extracellular matrix were formed after 14 days. On the other hand, after haSMC migration to the endothelial side had occurred, the addition of LDL and monocytes to cocultures with arterial media explants and haEC resulted in the formation of lipid-rich, low-cellular structures. After 28 days, characteristic in vitro plaque growth was induced; the plaque contained a lipid core with predominantly necrotic cells, extracellular lipid accumulations, atypically shaped lipid-loaded haSMC and macrophages, similar to in vivo foam cells, as well as an increased amount of extracellular matrix (collagen I, III and IV). These areas were surrounded by typical fibromuscular caps consisting of smooth muscle alpha-actin-positive haSMC. Finally, the formation of capillaries by haEC could also be observed within these structures.

Arteriosclerosis↗

Morphology of the peritoneal membrane during continuous ambulatory peritoneal dialysis.

In the last 3 years we performed 52 peritoneal biopsies (PB) in 31 patients on continuous ambulatory peritoneal dialysis (CAPD). Samples of the parietal peritoneum were obtained either during insertion of the catheter or while it was being repositioned or removed. PB was performed in 13 patients before initiating CAPD and in 27 after 7-49 months of CAPD while 7 had PB during peritonitis, and, again, in 5 of these cases, PB was repeated after 1-4 months for light, electron transmission, and scanning electron microscopy. BP after CAPD showed that mesothelial cells were irregularly spaced, and at times we observed alterations in the cellular structure. Rarely were these cells degenerating, while rarefaction and in many cases complete absence of microvilli were observed. In some cases the submesothelial layers showed rarefaction of the connective tissue and sclerosis. During peritonitis, PB showed more alterations with marked degeneration and in some cases necrosis of the mesothelium and alterations of connective tissue. PB performed some months after peritonitis showed only a partial regression of these alterations and sclerotic patches, and no microvilli were noted in the mesothelium.

Ascitic Fluid↗

Evolution of NMRI mice ovaries and corpora lutea during pregnancy: morphologic and morphometric study.

During pregnancy in mice, three groups of corpora lutea (CL) originating from 4 successive ovulatory cycles could be distinguished taking into account their size, cellular structure and stain affinity. Type I CL originated at the onset of pregnancy, type II CL originated during the 2 previous estrous cycles and type III CL were produced during a cycle preceding the two others. CL volume of type I increased 10-fold between day 0 and day 18.5, a 2.5-fold increase in volume occurred in type II CL between day 0 and day 3, although they derived from cycles preceding pregnancy. The volume of type III remained unchanged. This fact suggested that types I and II CL probably play a functional role in the ongoing pregnancy. After day 10 of pregnancy a high correlation coefficient (r = 0.933) is observed between type I CL and the number of embryos in the corresponding uterine horn.

Animals↗

Comparison of manual and automated methods of liquid-based cytology. A morphologic study.

OBJECTIVE: To evaluate the morphologic characteristics of gynecologic samples prepared by 3 different methods of liquid-based cytology. STUDY DESIGN: Cytologic samples from representative cases of each diagnostic category of squamous epithelial lesion, prepared by automated and manual liquid-based systems, were analyzed by 3 laboratories in the United States, Portugal and Brazil. The systems included: ThinPrep (automated, U.S. Food and Drug Administration approved; Cytyc Corp., Boxborough, Massachusetts, U.S.A.), Autocyte PREP (South American system, manual; TriPath Imaging, Inc., Burlington, North Carolina, U.S.A.) and DNACITOLIQ (manual; Digene Brazil, São Paulo, Brazil). A panel of 16 morphologic parameters was evaluated: cellularity, clean background, uniform distribution, artifacts, cellular overlapping, architectural and cytoplasmic distortion, cytoplasmic vacuolization, cellular elongation, imprecise cytoplasmic borders, folded cytoplasmic borders, nuclear hyperchromasia, coarse chromatin, prominent nucleolus, irregular nuclear borders, atypical mitosis and inflammatory infiltrate. Negative, atypical squamous cells of undetermined significance, low grade squamous intraepithelial lesion (LSIL) and high grade squamous intraepithelial lesion (HSIL) cases were included. Cases without biopsies were confirmed by consensus. RESULTS: Cellularity was adequate in all samples. Clean background was observed in the vast majority of samples with all liquid-based systems. Uniform distribution was frequently found in ThinPrep and Autocyte PREP samples but not in DNACITOLIQ. Artifacts were not present in DNACITOLIQ samples, rare in ThinPrep and observed in 8 (34.7%) Autocyte PREP. Cellular overlapping was observed in all 3 system samples: 11 (31.42%) cases in ThinPrep, 16 (69.56%) in Autocyte PREP and 17 (68%) in DNACITOLIQ System. Architectural and cytoplasmic distortion were present in 3 cases of HSIL (13%) and cytoplasmic vacuolization in 2 cases of LSIL and 1 HSIL of Autocyte PREP. Cellular elongation was found in 13 (56.5%) Autocyte PREP and in 5 (20%) DNACITOLIQ samples. Inflammatory infiltrate was found in all 3 system samples but with more frequency in the Autocyte PREP (69.56%) and DNACITOLIQ System (72%). CONCLUSION: This study clearly indicated that in spite of the different methodologies, the 3 methods adequately preserved cellular structure for morphologic evaluation. The choice of method will depend on price, availability and procedures involved.

Artifacts↗

Mechanisms, pathophysiology, and therapy of arterial stiffness.

Arterial stiffness is a growing epidemic associated with increased risk of cardiovascular events, dementia, and death. Decreased compliance of the central vasculature alters arterial pressure and flow dynamics and impacts cardiac performance and coronary perfusion. This article reviews the structural, cellular, and genetic contributors to arterial stiffness, including the roles of the scaffolding proteins, extracellular matrix, inflammatory molecules, endothelial cell function, and reactive oxidant species. Additional influences of atherosclerosis, glucose regulation, chronic renal disease, salt, and changes in neurohormonal regulation are discussed. A review of the hemodynamic impact of arterial stiffness follows. A number of lifestyle changes and therapies that reduce arterial stiffness are presented, including weight loss, exercise, salt reduction, alcohol consumption, and neuroendocrine-directed therapies, such as those targeting the renin-angiotensin aldosterone system, natriuretic peptides, insulin modulators, as well as novel therapies that target advanced glycation end products.

Arteries↗

Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology.

Myocardial infarction is the most frequent cause of mortality in the United States as well as in most western countries. In this review, the processes leading to myocardial infarction are described based on the most recent studies of vascular biology; in addition, evolving strategies for prevention are outlined. The following was specifically discussed. (1) Five phases of the progression of coronary atherosclerosis (phases 1 to 5) and eight morphologically different lesions (types I, II, III, IV, Va, Vb, Vc, and VI) in the various phases are defined. (2) The present understanding of the pathogenesis of each of the phases of progression and of the various lesion types preceding myocardial infarction is described; particular emphasis is placed on the physical, structural, cellular, and chemical characteristics of the "vulnerable or unstable plaques" prone to disruption (types IV and Va lesions). (3) The fate of plaque disruption (type VI lesion) in the genesis of the various coronary syndromes and especially acute myocardial infarction is defined; particular emphasis is placed on the combination of plaque disruption and a high thrombogenic risk profile--local factors (ie, degree of plaque disruption, exposure of lipid-macrophage-rich plaque, etc) and systemic factors (ie, catecholamines, RAS, fibrinogen, etc)--in the genesis of myocardial infarction. (4) Strategies of regression or stabilization of "vulnerable or unstable plaques" for prevention of myocardial infarction are presented within the context of recent favorable experience with risk factor modification and lipid-modifying angiographic trials, beta-blockade and angiotensin-converting enzyme inhibition, antithrombotic strategies, and the possible role of estrogens. The recent past has been very fruitful in yielding a better understanding of the processes leading to myocardial infarction, and the near future appears very promising in terms of preventing the number 1 killer in the western world.

Coronary Artery Disease↗

Role of protein kinase C in mitochondrial KATP channel-mediated protection against Ca2+ overload injury in rat myocardium.

Growing evidence exists that ATP-sensitive mitochondrial potassium channels (MitoKATP channel) are a major contributor to the cardiac protection against ischemia. Given the importance of mitochondria in the cardiac cell, we tested whether the potent and specific opener of the MitoKATP channel diazoxide attenuates the lethal injury associated with Ca2+overload. The specific aims of this study were to test whether protection by diazoxide is mediated by MitoKATP channels; whether diazoxide mimics the effects of Ca2+ preconditioning; and whether diazoxide reduces Ca2+ paradox (PD) injury via protein kinase C (PKC) signaling pathways. Langendorff-perfused rat hearts were subjected to the Ca2+ PD (10 minutes of Ca2+ depletion followed by 10 minutes of Ca2+ repletion). The effects of the MitoKATP channel and other interventions on functional, biochemical, and pathological changes in hearts subjected to Ca2+ PD were assessed. In hearts treated with 80 micromol/L diazoxide, left ventricular end-diastolic pressure and coronary flow were significantly preserved after Ca2+ PD; peak lactate dehydrogenase release was also significantly decreased, although ATP content was less depleted. The cellular structures were well preserved, including mitochondria and intercalated disks in diazoxide-treated hearts compared with nontreated Ca2+ PD hearts. The salutary effects of diazoxide on the Ca2+ PD injury were similar to those in hearts that underwent Ca2+ preconditioning or pretreatment with phorbol 12-myristate 13-acetate before Ca2+ PD. The addition of sodium 5-hydroxydecanoate, a specific MitoKATP channel inhibitor, or chelerythrine chloride, a PKC inhibitor, during diazoxide pretreatment completely abolished the beneficial effects of diazoxide on the Ca2+ PD. Blockade of Ca2+ entry during diazoxide treatment by inhibiting L-type Ca2+ channel with verapamil or nifedipine also completely reversed the beneficial effects of diazoxide on the Ca2+ PD. PKC-delta was translocated to the mitochondria, intercalated disks, and nuclei of myocytes in diazoxide-pretreated hearts, and PKC-alpha and PKC-epsilon were translocated to sarcolemma and intercalated disks, respectively. This study suggests that the effect of the MitoKATP channel is mediated by PKC-mediated signaling pathway.

Adenosine Triphosphate↗

The perfect C. elegans project: an initial report.

The soil nematode Caenorhabditis Elegans (C. elegans) is the most investigated of all multicellular organisms. Since the proposal to use it as a model organism, a series of research projects have been undertaken, investigating various aspects of this organism. As a result, the complete cell lineage, neural circuitry, and various genes and their functions have been identified. The complete C. elegans DNA sequencing and gene expression mapping for each cell at different times during embryogenesis will be identified in a few years. Given the abundance of collected data, we believe that the time is ripe to introduce synthetic models of C. elegans to further enhance our understanding of the underlying principles of its development and behavior. For this reason, we have started the Perfect C. elegans Project, which aims to produce ultimately a complete synthetic model of C. elegans' cellular structure and function. This article describes the goal, the approach, and the initial results of the project.

Animals↗