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Mewada, Shivlal, Pradeep Sharma, and S. S. Gautam. "Investigation of Efficient Cryptic Algorithm for Text using SM Crypter." International Journal of Information Science and Computing 3, no. 2 (2016): 99. http://dx.doi.org/10.5958/2454-9533.2016.00012.0.
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Brochet, Laura. "D�crypter, comprendre�et ma�triser sa pr�sence en ligne." L'Observatoire N�47, no. 1 (2016): 94. http://dx.doi.org/10.3917/lobs.047.0094.
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Brisset, Annie. "Traduire le texte dans son projet. Le littéralisme est soluble dans la poésie moderne : Auden." TTR : traduction, terminologie, rédaction 12, no. 2 (2007): 39–56. http://dx.doi.org/10.7202/037370ar.
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Résumé Traduire le texte dans son projet. Le littéralisme est soluble dans la poésie moderne : Auden — Bien qu'il soit reconnu comme l'un des plus grands poètes du XXe siècle, W. H. Auden est peu traduit en français. Son oeuvre, il est vrai, résiste à la traduction lorsqu'elle s'amuse, comme dans le poème qui sert ici d'exemple, à crypter le langage de tous les jours en le coulant dans une forme contrainte par la tradition. « The Three Companions » est un poème clé dans l'oeuvre d'Auden qui le publie au début des années trente et le reconduit dans plusieurs de ses recueils. Nous en proposons une analyse qui ouvre un dialogue avec chacune des traductions (une dizaine) et avec les commentaires qui les accompagnent.
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Bachmann, O., B. Riederer, H. Rossmann, et al. "The Na+/H+ exchanger isoform 2 is the predominant NHE isoform in murine colonic crypts and its lack causes NHE3 upregulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 1 (2004): G125—G133. http://dx.doi.org/10.1152/ajpgi.00332.2003.
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The Na+/H+ exchanger isoform NHE2 is highly expressed in the intestinal tract, but its physiological role has remained obscure. The aim of this study was to define its expression, location, and regulatory properties in murine colon and to look for the compensatory changes in NHE2 (−/−) colon that allow normal histology and absorptive function. To this end, we measured murine proximal colonic surface and crypt cell NHE1, NHE2, and NHE3 expression levels, transport rates in response to acid, hyperosmolarity and cAMP in murine proximal colonic crypts, as well as changes in transcript levels and acid-activated NHE activity in NHE2 (−/−) crypts. We found that NHE2 was expressed most abundantly in crypts, NHE1 equally in crypts and surface cells, and NHE3 much stronger in surface cells. NHE2, like NHE1, was activated by low intracellular pH (pHi), hyperosmolarity, and cAMP, whereas NHE3 was activated only by low pHi. Crypts isolated from NHE2 (−/−) mice displayed increased acid-activated NHE1- and NHE3-attributable Na+/H+ exchange activity, no change in NHE1 expression, and NHE3 expression levels twice as high as in normal littermates. No change in cellular ultrastructure was found in NHE2 (−/−) colon. Our results demonstrate high NHE2 expression in the crypts and suggest a role for NHE2 in cryptal pHi and volume homeostasis.
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Baker, Ann-Marie, Calum Gabbutt, Marc J. Williams, et al. "Crypt fusion as a homeostatic mechanism in the human colon." Gut 68, no. 11 (2019): 1986–93. http://dx.doi.org/10.1136/gutjnl-2018-317540.
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ObjectiveThe crypt population in the human intestine is dynamic: crypts can divide to produce two new daughter crypts through a process termed crypt fission, but whether this is balanced by a second process to remove crypts, as recently shown in mouse models, is uncertain. We examined whether crypt fusion (the process of two neighbouring crypts fusing into a single daughter crypt) occurs in the human colon.DesignWe used somatic alterations in the gene cytochrome c oxidase (CCO) as lineage tracing markers to assess the clonality of bifurcating colon crypts (n=309 bifurcating crypts from 13 patients). Mathematical modelling was used to determine whether the existence of crypt fusion can explain the experimental data, and how the process of fusion influences the rate of crypt fission.ResultsIn 55% (21/38) of bifurcating crypts in which clonality could be assessed, we observed perfect segregation of clonal lineages to the respective crypt arms. Mathematical modelling showed that this frequency of perfect segregation could not be explained by fission alone (p<10−20). With the rates of fission and fusion taken to be approximately equal, we then used the distribution of CCO-deficient patch size to estimate the rate of crypt fission, finding a value of around 0.011 divisions/crypt/year.ConclusionsWe have provided the evidence that human colonic crypts undergo fusion, a potential homeostatic process to regulate total crypt number. The existence of crypt fusion in the human colon adds a new facet to our understanding of the highly dynamic and plastic phenotype of the colonic epithelium.
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Li, Y. Q., S. A. Roberts, U. Paulus, M. Loeffler, and C. S. Potten. "The crypt cycle in mouse small intestinal epithelium." Journal of Cell Science 107, no. 12 (1994): 3271–79. http://dx.doi.org/10.1242/jcs.107.12.3271.
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We have used a mutation-induced marker system in the intestine of mice heterozygous at the Dlb-1 locus, which determines the expression of binding sites for the lectin Dolichos biflorus agglutinin, and the frequency of clustering of mutated crypts with time as a means of investigating the frequency of the crypt fission process and the crypt cycle. Whole-mount preparations from heterozygous Dlb-1b/Dlb-1a mice were stained with a peroxidase conjugate of Dolichos biflorus agglutinin. Mutations at the Dlb-1b locus in crypt stem cells result in loss of DBA-Px binding in these cells and subsequently their progeny, which eventually results in a rare isolated single, unstained crypt. The subsequent development of pairs, triplets and clusters of negative staining crypts has been assumed to be the result of crypt fission. The frequency of these fission events has been measured in control untreated mice. These negative crypts are the result of spontaneous mutations. We have also looked at mutated crypts after treatment with N-nitroso-N-ethylurea or N-methyl-N'-nitro-N-nitrosoguanidine of young adult mice, which elevates the number of mutations. Our results suggest that the crypt cycle in control animals is very long, 187 +/- 44 weeks (3.6 years, i.e. essentially the life of a laboratory mouse). This implies that about a third of the crypts may divide once in the life of a mouse. After sufficient time for conversion of mixed crypts to monophenotypic crypts after mutagen treatment several clusters of negative crypts were seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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Zaborin, Alexander, Monika Krezalek, Sanjiv Hyoju, et al. "Critical role of microbiota within cecal crypts on the regenerative capacity of the intestinal epithelium following surgical stress." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 2 (2017): G112—G122. http://dx.doi.org/10.1152/ajpgi.00294.2016.
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Cecal crypts represent a unique niche that are normally occupied by the commensal microbiota. Due to their density and close proximity to stem cells, microbiota within cecal crypts may modulate epithelial regeneration. Here we demonstrate that surgical stress, a process that invariably involves a short period of starvation, antibiotic exposure, and tissue injury, results in cecal crypt evacuation of their microbiota. Crypts devoid of their microbiota display pathophysiological features characterized by abnormal stem cell activation as judged by leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5) staining, expansion of the proliferative zone toward the tips of the crypts, and an increase in apoptosis. In addition, crypts devoid of their microbiota display loss of their regenerative capacity as assessed by their ability to form organoids ex vivo. When a four-member human pathogen community isolated from the stool of a critically ill patient is introduced into the cecum of mice with empty crypts, crypts become occupied by the pathogens and further disruption of crypt homeostasis is observed. Fecal microbiota transplantation restores the cecal crypts’ microbiota, normalizes homeostasis within crypts, and reestablishes crypt regenerative capacity. Taken together, these findings define an emerging role for the microbiota within cecal crypts to maintain epithelial cell homeostasis in a manner that may enhance recovery in response to the physiological stress imposed by the process of surgery. NEW & NOTEWORTHY This study provides novel insight into the process by which surgical injury places the intestinal epithelium at risk for colonization by pathogenic microbes and impairment of its regenerative capacity via loss of its microbiota. We show that fecal transplant restores crypt homeostasis in association with repopulation of the microbiota within cecal crypts.
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Schmidt, G. H., D. J. Winton, and B. A. Ponder. "Development of the pattern of cell renewal in the crypt-villus unit of chimaeric mouse small intestine." Development 103, no. 4 (1988): 785–90. http://dx.doi.org/10.1242/dev.103.4.785.
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We have previously shown that the epithelium of each adult intestinal crypt in chimaeric mice is derived from a single progenitor cell. Whether the crypts are monoclonal from the outset-that is, are formed by the proliferation of a single cell-or whether their formation is initiated by several cells was not known. Here we report that many crypts contain cells of both chimaeric genotypes in the neonatal period indicating a polyclonal origin at this stage of morphogenesis. The cellular organization of the early neonatal crypt is therefore different from that of the adult crypt, which includes a zone of ‘anchored’ stem cells above the crypt base. Within 2 weeks, however, the crypt progenitor cell and its descendants displace all other cells from the crypt and the crypt attains monoclonality. The distribution of enterocytes on chimaeric villi in the neonate shows a mottled pattern of mosaicism which is progressively replaced by coherent sheets of cells from the crypts, and within two weeks the orderly adult clonal pattern is established.
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Merritt, A. J., C. S. Potten, A. J. Watson, et al. "Differential expression of bcl-2 in intestinal epithelia. Correlation with attenuation of apoptosis in colonic crypts and the incidence of colonic neoplasia." Journal of Cell Science 108, no. 6 (1995): 2261–71. http://dx.doi.org/10.1242/jcs.108.6.2261.
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The cell-positional incidence of both spontaneous and damage-induced apoptosis of epithelial cells was assessed in longitudinal sections of the crypts of small intestine and colon of BDF1 mice. This was compared, using immunohistochemistry, with the pattern of expression of bcl-2, a suppressor of apoptosis. In the small intestine, apoptosis was maximal around cell position 4 from the base of the crypt; this closely corresponds to the position considered to contain the stem cells. In the colon, however, apoptosis was not confined to the area considered to harbour the stem cells (position 1 and 2). Instead, apoptosis was attenuated and distributed along the length of the crypt. Some cells at the base of murine colonic crypts expressed bcl-2 protein, whereas bcl-2 was absent in the crypts of the small intestine. Most pertinently, bcl-2 was absent from small intestinal crypt cells at positions 4–5 (the stem cell region). The importance of the expression of bcl-2 to the attenuation of apoptosis in stem cells was confirmed by analysis of the levels of both spontaneous and induced apoptosis in homozygously bcl-2 null C57BL/6 mice: in colonic crypts the level of spontaneous apoptosis rose significantly, and selectively at the base of the crypt, in comparison with crypts from wild-type animals. In contrast, there was no rise in spontaneous apoptosis in the small intestinal crypts from the bcl-2 null animals. Analysis of sections of human colon and small intestine also showed that expression of bcl-2 was confined to the base of the colonic crypt. The attenuation of apoptosis by bcl-2 in the region of the stem cells of the colonic crypts may dispose these to neoplastic transformation. Indeed, analysis of human carcinomas revealed expression of bcl-2, which in some samples was reciprocal with the expression of p53.
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Muncan, Vanesa, Owen J. Sansom, Leon Tertoolen, et al. "Rapid Loss of Intestinal Crypts upon Conditional Deletion of the Wnt/Tcf-4 Target Gene c-Myc." Molecular and Cellular Biology 26, no. 22 (2006): 8418–26. http://dx.doi.org/10.1128/mcb.00821-06.
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ABSTRACT Inhibition of the mutationally activated Wnt cascade in colorectal cancer cell lines induces a rapid G1 arrest and subsequent differentiation. This arrest can be overcome by maintaining expression of a single Tcf4 target gene, the proto-oncogene c-Myc. Since colorectal cancer cells share many molecular characteristics with proliferative crypt progenitors, we have assessed the physiological role of c-Myc in adult crypts by conditional gene deletion. c-Myc-deficient crypts are lost within weeks and replaced by c-Myc-proficient crypts through a fission process of crypts that have escaped gene deletion. Although c-Myc − / − crypt cells remain in the cell cycle, they are on average much smaller than wild-type cells, cycle slower, and divide at a smaller cell size. c-Myc appears essential for crypt progenitor cells to provide the necessary biosynthetic capacity to successfully progress through the cell cycle.
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Oliveira, E. P., and G. Romanazzi. "Modeling and Computer Simulation of Viscoelastic Crypt Deformation." Trends in Computational and Applied Mathematics 23, no. 1 (2022): 193–211. http://dx.doi.org/10.5540/tcam.2022.023.01.00193.
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Colorectal cancer morphogenesis begins at the cellular level from cell mutations in the intestinal epithelium cavities called crypts. These mutations lead to a pressure difference in the epithelium crypt walls, which causes deformation and generates visible abnormalities in the epithelium. The geometrical modeling of these crypts and the mathematical modeling of the physical process that cause the deformations can be simulated by using a Finite Element Method. The method solves numerically the system of PDE equations that governs this phenomenon and permits to estimate the deformations of the crypt walls. We simulate in this work the crypt deformation when the cell mutations appear in several regions of the crypt epithelium.
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Martin, K., C. S. Potten, S. A. Roberts, and T. B. Kirkwood. "Altered stem cell regeneration in irradiated intestinal crypts of senescent mice." Journal of Cell Science 111, no. 16 (1998): 2297–303. http://dx.doi.org/10.1242/jcs.111.16.2297.
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Ageing is associated with a progressive deterioration in the functions of many organs within the body. In tissue with high cell turnover, the maintenance of the stem cells is of particular importance. Any accumulation of damage in stem cells may affect their function and hence threaten the homeostasis and regenerative capacity of the tissue. The small intestine represents a good model for the study of stem cells because of its spatial and hierarchical organisation. We have examined the effect of age on stem cell regenerative capacity after irradiation, using the microcolony assay. Crypt survival levels, the growth rate of surviving crypts, and the number of cells able to repopulate a crypt have been investigated by irradiating groups of 6–7 month old and 28–30 month old ICRFa male mice. After high doses of irradiation, the surviving crypts in old mice were both smaller and fewer in number than in young mice. The growth rate of surviving crypts was determined by measuring the crypt area and the number of cells/crypt at various times after 14 Gy irradiation. There was a growth delay of between about one half and one day in the older mice. Surprisingly, the number of clonogenic cells per crypt was estimated to be greater in the older mice. These studies indicate important age-related alterations in the capacity to regenerate the crypts after radiation damage.
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GARCIA, BRENDA, MINA ELMIRY, JONATHAN A MOORE, ZEIN KATTIH, and PRIYANKA MAKKAR. "CRYPTIC CRYPTO: PULMONARY CRYPTOCOCCOSIS IN AN IMMUNOCOMPETENT HOST." Chest 162, no. 4 (2022): A575. http://dx.doi.org/10.1016/j.chest.2022.08.446.
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Abrahamse, S. L., A. Vis, R. J. Bindels, and C. H. van Os. "Regulation of intracellular pH in crypt cells from rabbit distal colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 3 (1994): G409—G415. http://dx.doi.org/10.1152/ajpgi.1994.267.3.g409.
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H+ secretory mechanisms and intrinsic intracellular buffering capacity were studied in crypt cells from rabbit distal colon. To this end crypts of Lieberkuhn were isolated by microdissection, and intracellular pH (pHi) was measured using digital imaging fluorescence microscopy and the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)- 5(6)-carboxyfluorescein. In the absence of HCO(3-)-CO2 and presence of Na+, resting pHi was 7.51 +/- 0.04 (n = 237/23, cells/crypts). However, 6 min after superfusion with a solution containing zero Na+, 1 x 10(5) M Sch-28080 and 5 x 10(-8) M bafilomycin A1, pHi in cells at the bottom of the crypts was significantly reduced, whereas pHi in cells at the top of the crypts remained unchanged. The intrinsic buffering capacity of cells from the middle to the top portion of crypts was significantly higher in the pHi range 7.2-7.6 than of cells at the bottom of the crypt. H+ secretion after an NH(4+)-NH3 pulse amounted to 245 +/- 53 microM/s (n = 73/7) at pHi 7.1 and was largely Na+ dependent and ethylisopropylamiloride sensitive. The Na(+)-independent recovery of pHi after an acid load was insensitive to Sch-28080 and bafilomycin A1. In conclusion, pHi in colonic crypt cells is regulated through Na+/H+ exchange activity in the absence of HCO3-. In addition, intracellular buffering capacity varied with the position along the crypt axis, whereas Na+/H+ exchange activity and pHi did not.
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Howard, R. Logan, Yuli Wang, and Nancy L. Allbritton. "Use of liquid lithography to form in vitro intestinal crypts with varying microcurvature surrounding the stem cell niche." Journal of Micromechanics and Microengineering 31, no. 12 (2021): 125006. http://dx.doi.org/10.1088/1361-6439/ac2d9c.
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Abstract Objective. The role of the crypt microarchitecture and surrounding tissue curvature on intestinal stem/proliferative cell physiology is unknown. The utility of liquid lithography in creating polydimethylsiloxane (PDMS) micropillar stamps with controlled tip curvature was assessed. Using these stamps, the impact of microcurvature at the crypt base on intestinal cell and cytoskeletal behavior was studied. Approach. An SU-8 master mold as a support, polyols of varying surface energies as sacrificial liquids, and liquid PDMS as the solidifiable material were combined using liquid lithography to form PDMS micropillar arrays. Vapor phase deposition of organosilane onto the master mold was used to modify the surface energy of the master mold to shape the micropillar tips. Collagen was molded using the micropillar arrays forming a scaffold for culture of human primary colonic epithelial cells. Cell proliferation and cytoskeletal properties were assessed using fluorescent stains. Main results. Liquid lithography using low surface energy polyols (<55 dynes cm−1) generated convex-tipped PDMS micropillars, while polyols with higher surface energies (>55 dynes cm−1) yielded concave-tipped PDMS micropillars. Gradients of octyltrichlorosilane deposition across a master mold with an array of microwells yielded a PDMS micropillar array with a range of tip curvatures. Human primary colonic epithelial cells cultured on micropillar-molded collagen scaffolds demonstrated a stem/proliferative cell compartment at the crypt base. Crypts with a convex base demonstrated significantly lower cell proliferation at the crypt base than that of cells in crypts with either flat or concave bases. Crypts with a convex base also displayed higher levels of G-actin activity compared to that of crypts with flat or concave bases. Significance. Liquid lithography enabled creation of arrays of in vitro colonic crypts with programmable curvature. Primary cells at the crypt base sensed and responded to surface curvature by altering their proliferation and cytoskeletal properties.
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Chandrakesan, Parthasarathy, Ishfaq Ahmed, Anisha Chinthalapally та ін. "Distinct Compartmentalization of NF-κB Activity in Crypt and Crypt-Denuded Lamina Propria Precedes and Accompanies Hyperplasia and/or Colitis following Bacterial Infection". Infection and Immunity 80, № 2 (2011): 753–67. http://dx.doi.org/10.1128/iai.06101-11.
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ABSTRACTCitrobacter rodentiuminduces transmissible murine colonic hyperplasia (TMCH) and variable degrees of inflammation and necrosis depending upon the genetic background. UtilizingC. rodentium-induced TMCH in C3H/HeNHsd inbred mice, we observed significant crypt hyperplasia on days 3 and 7 preceding active colitis. NF-κB activity in the crypt-denuded lamina propria (CLP) increased within 24 h postinfection, followed by its activation in the crypts at day 3, which peaked by day 7. Increases in interleukin-α1 (IL-1α), IL-12(p40), and macrophage inflammatory protein 1α (MIP-1α) paralleled NF-κB activation, while increases in IL-1α/β, IL-6/IL-12(p40)/granulocyte colony-stimulating factor (G-CSF)/keratinocyte-derived chemokine (KC)/monocyte chemotactic protein 1 (MCP-1), and MIP-1α followed NF-κB activation leading to significant recruitment of neutrophils to the colonic mucosa and increased colonic myeloperoxidase (MPO) activity. Phosphorylation of the crypt cellular and nuclear p65 subunit at serines 276 and 536 led to functional NF-κB activation that facilitated expression of its downstream target, CXCL-1/KC, during TMCH. Distinct compartmentalization of phosphorylated extracellular signal-regulated kinase 1 and 2 ([ERK1/2] Thr180/Tyr182) and p38 (Thr202/Tyr204) in the CLP preceded increases in the crypts. Inhibition of ERK1/2 and p38 suppressed NF-κB activity in both crypts and the CLP. Dietary administration of 6% pectin or 4% curcumin inC. rodentium-infected mice also inhibited NF-κB activity and blocked CD3, F4/80, IL-1α/β, G-CSF/MCP-1/KC, and MPO activity in the CLP while not affecting NF-κB activity in the crypts. Thus, distinct compartmentalization of NF-κB activity in the crypts and the CLP regulates crypt hyperplasia and/or colitis, and dietary intervention may be a novel strategy to modulate NF-κB-dependent protective immunity to facilitate crypt regeneration followingC. rodentium-induced pathogenesis.
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Houchen, Courtney W., Mark A. Sturmoski, Shrikant Anant, Richard M. Breyer, and William F. Stenson. "Prosurvival and antiapoptotic effects of PGE2in radiation injury are mediated by EP2 receptor in intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 3 (2003): G490—G498. http://dx.doi.org/10.1152/ajpgi.00240.2002.
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The biological activities of PGE2 are mediated through EP receptors (EP1–EP4), plasma membrane G protein-coupled receptors that differ in ligand binding and signal-transduction pathways. We investigated gastrointestinal EP2 receptor expression in adult mice before and after radiation injury and evaluated intestinal stem cell survival and crypt epithelial apoptosis after radiation injury in EP2 null mice. EP2 was expressed throughout the gut. Intestinal EP2 mRNA increased fivefold after γ-irradiation. Crypt survival was diminished in EP2 −/− mice (4.06 crypts/cross section) compared with wild-type littermates (8.15 crypts/cross section). Radiation-induced apoptosis was significantly increased in EP2 −/− mice compared with wild-type littermates. Apoptosis was 1.6-fold higher in EP2 −/− mice (5.9 apoptotic cells/crypt) than in wild-type mice (3.5 apoptotic cells/crypt). The EP2receptor is expressed in mouse gastrointestinal epithelial cells and is upregulated following radiation injury. The effects of PGE2on both crypt epithelial apoptosis and intestinal crypt stem cell survival are mediated through the EP2 receptor.
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Feinman, Rena, Iriana Colorado, Jenny Zilberberg, et al. "Intestinal Epithelial HIF-1 Plays a Protective Role in Gut Graft Versus Host Disease." Blood 124, no. 21 (2014): 539. http://dx.doi.org/10.1182/blood.v124.21.539.539.
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Abstract Acute graft-versus-host disease (GVHD) is a major cause of nonrelapse morbidity and mortality following allogeneic blood and marrow transplantation (BMT). The majority of studies delineating the mechanisms involved in GVHD have focused on the alloreactive T cell response and their downstream cellular and inflammatory effector phases. While these efforts have provided important mechanistic insights that have been translated into therapies that target the T cell compartment, they ignore the role that the target organ plays in both initiating and propagating this disease. Acute gut GVHD affects more than 60% of patients and is a leading cause of death. The mechanisms for the early, conditioning-related, intestinal injuries that are the precipitating event leading to GVHD or how subsequent gut-specific GVHD actually disrupts intestinal homeostasis have not been fully explored. The transcription factor, hypoxia inducible factor-1 (HIF-1) has emerged as a common denominator for hypoxia and inflammation. Given that inflammatory bowel disease (IBD) and GVHD share many pathogenic mechanisms and intestinal epithelial HIF-1α afforded protection in IBD models, we hypothesize that the persistent activation of HIF-1 will protect the intestinal epithelium from radiation/chemotherapy and alloreactive T cell-induced damage. Since crypt damage is a hallmark of gut GVHD, we first determined whether loss of intestinal epithelial HIF-1α impaired intestinal regeneration after GVHD damage using conditional HIF-1α (HIF-1αIE) knockout mice that lack HIF-1α in the intestinal epithelium. In a major MHC mismatched B10.BR (H2k) into B6 (H2b) GVHD model, 8 days post-BMT, histopathologic assessment of H&E stained ileums of HIF-1αIE mice showed more severe crypt damage, loss of Paneth cells and fewer regenerating crypts as compared to wild-type (WT) mice. A two-fold increase of aberrant mitoses (p<0.02 vs WT) was observed in crypts of HIF-1αIE mice. Consistent with these findings, real-time PCR analysis demonstrated that loss of epithelial HIF-1α did not induce the expression of Lgr5 mRNA levels (p<0.05) and reduced Reg3γ mRNA levels in the ileum by 2.4-fold (p<0.05) relative to WT mice, post-BMT. Since intestinal crypts have been shown to undergo extensive proliferation to repair damage following injury, we examined the crypt proliferative response 21 days post-BMT using immunohistochemistry for the proliferative marker Ki67. Hyperplastic elongated crypts that are characteristic of regenerating crypts after radiation-induced damage were observed in Ki67-stained ileal sections of WT mice post-BMT whereas smaller "aberrant" appearing crypts with asymmetrically distributed Ki67-labeled cells and fewer regenerating crypts were evident in HIF-1αIE mice post-BMT. In control WT and HIF-1αIE (receiving T cell depleted BM), Ki67+-proliferating cells resided at the crypt base. The extent of irregular distribution of Ki67 within 50 crypts/ileum was graded independently with a grading score ranging 0 to 3 (0 = limited to the base of crypt, 1= symmetric distribution at crypt base and along each side of the elongated crypt, 2 = asymmetric distribution in bottom 2/3 of crypt and 3 = asymmetric distribution of Ki67-labeled cells in entire crypt without lumen). A modest but significant increase in the aberrant proliferative score was 1.72 in the HIF-1αIE post-BMT group versus 1.46 in the WT post-BMT group (p<0.05). Taken together, our findings suggest that intestinal epithelial HIF-1 may protect the intestinal stem cell niche and preserve intestinal regeneration in response to gut GVHD. Disclosures No relevant conflicts of interest to declare.
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Hirokawa, Yumiko, Kelvin Hon Yan Yip, Chin Wee Tan, and Antony W. Burgess. "Colonic myofibroblast cell line stimulates colonoid formation." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 7 (2014): G547—G556. http://dx.doi.org/10.1152/ajpgi.00267.2013.
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A stable and efficient system for the culture of murine colon epithelial cells or crypts is required to facilitate studies of the dynamics and factors affecting colon stem cell niche and crypt formation. Survival of colonic epithelial cells or crypts in vitro was not established until recently, when it was found that exogenous Wnt3A and R-spondin could promote cell survival and formation of spheroids (colonospheres) or some advanced organoids with well-developed crypts (colonoids). However, after 6–8 days in these culture conditions, only small numbers of colonospheres form organoids with crypt-like structures (colonoids). This study describes the use of a myofibroblast cell line and a coculture system that increases the efficiency of colonoid formation from isolated crypts. The enhanced coculture system has significantly improved colonoid-forming efficiency compared with results from previous systems. Crypt formation can be detected as early as day 2. The coculture system will facilitate the characterization of the colon stem cell niche and the changes that occur as a result of perturbations or mutations in colon stem or epithelial cells, such as those that favor precancerous adenoma or cancer.
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Ströbl, Regina, and Andreas Ströbl. "“…a Gentle Calm and Happy Resurrection” – Theological and Folk-religious Backgrounds of Crypt Burials." Acta Universitatis Lodziensis. Folia Archaeologica, no. 35 (December 30, 2020): 7–17. http://dx.doi.org/10.18778/0208-6034.35.01.
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For years there has been a lively discussion if there did exist a tradition of intentional mummification in Christian Europe, since hundreds of naturally mummified individuals of a social elite have been found preserved in family- and church crypts. But in most cases well ventilated crypt spaces are the reason for this natural mummification. Besides their dynastic and representative nature, crypts with the well closed coffins were probably understood as spaces of protection for a facilitated resurrection of the body at the day of judgement. Physical resurrection was church-dogmatical from the beginning of Christianity until 20th century and as well a private religious fact. Numerous inscriptions on coffins and crypt walls testify the hope of a “happy resurrection”. The believe in resurrection is common for all confessions, though it is probably Protestantism that has promoted burials in crypts. But only the comprehension of the interaction of different social and religious aspects opens the access to the complex “crypt”.
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Kobluk, David R., and Mary A. Lysenko. "Hurricane effects on shallow-water cryptic reef molluscs, Fiji Islands." Journal of Paleontology 67, no. 5 (1993): 798–816. http://dx.doi.org/10.1017/s0022336000037069.
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An assemblage of 343 species of cryptic, shelled molluscs was identified in three large samples from shallow subtidal and intertidal shelter habitats under rubble and corals at Malololailai Fiji in 1983, 1984, and 1985. One species was a polyplacophoran, 273 were gastropods (38 families), and 69 were bivalves (21 families). Cryptic gastropods were more abundant than bivalves, but showed a reduction in abundance relative to bivalves from 1983 to 1985. The abundances of many cryptic molluscs show dramatic adjustments from 1983 to 1985, chiefly due to hurricanes in 1983 and 1985, showing a decrease in equitability with increased physical disturbance. The abundance and diversity of molluscan predators in the crypts means that predation in these habitats may be substantial.The gastropod sample diversity showed the greatest change during the 1984 post-hurricane recovery period. The 1985 hurricanes affected the sample diversity by shifting the gastropod diversity closer to what it was after the 1983 hurricane. The bivalves underwent a similar shift in sample diversity, although larger numbers of individuals in proportionately more species survived the hurricanes.The cryptic bivalves exploited space in new crypts, while maintaining their rate of increase in abundance in the recovery period after the 1983 hurricane and through the two hurricanes in 1985. The gastropods declined in abundance after the 1983 hurricane. They recovered after the 1985 hurricanes by doubling their abundance, showing that they could exploit new resources in crypts. This increase in the gastropod population was not proportional to the increase in available cryptic space. This may mean they were still recovering in August 1985, or they may have been unable to capture their portion of cryptic space in competition with other organisms during recovery.The 1985 hurricanes did not have much effect on the overall molluscan diversity, a possible result of pruning by the 1983 hurricane of molluscs unable to survive storms. Because there was only a short interval between the hurricanes, many molluscs that survived the 1983 event were still in the population, so that the cryptic molluscs probably were better able to deal with the effects of the 1985 hurricanes than they would have been before the 1983 hurricane. The result was that the sample diversity after the 1983 hurricane increased during the recovery period but did not decline later even though the population was devastated by hurricanes in 1985. This lends support to intermediate disturbance models linking increasing or stable diversity with disturbances spaced at intervals allowing recovery.
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Liu, Jinghua, Nancy M. Walker, Matthew T. Cook, Akifumi Ootani, and Lane L. Clarke. "Functional Cftr in crypt epithelium of organotypic enteroid cultures from murine small intestine." American Journal of Physiology-Cell Physiology 302, no. 10 (2012): C1492—C1503. http://dx.doi.org/10.1152/ajpcell.00392.2011.
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Physiological studies of intact crypt epithelium have been limited by problems of accessibility in vivo and dedifferentiation in standard primary culture. Investigations of murine intestinal stem cells have recently yielded a primary intestinal culture in three-dimensional gel suspension that recapitulates crypt structure and epithelial differentiation (Sato T, Vries RG, Snippert HJ, van de Wetering M, Barker N, Stange DE, Van Es JH, Abo A, Kujala P, Peters PJ, Clevers H. Nature 459: 262–265, 2009). We investigated the utility of murine intestinal crypt cultures (termed “enteroids”) for physiological studies of crypt epithelium by focusing on the transport activity of the cystic fibrosis transmembrane conductance regulator Cftr. Enteroids had multiple crypts with well-differentiated goblet and Paneth cells that degranulated on exposure to the muscarinic agonist carbachol. Modified growth medium provided a crypt proliferation rate, as measured by 5-ethynyl-2′-deoxyuridine labeling, which was similar to proliferation in vivo. Immunoblots demonstrated equivalent Cftr expression in comparisons of freshly isolated crypts with primary and passage 1 enteroids. Apparent enteroid differences in mRNA expression of other transporters were primarily associated with villous epithelial contamination of freshly isolated crypts. Microelectrode analysis revealed cAMP-stimulated membrane depolarization in enteroid epithelium from wild-type (WT) but not Cftr knockout (KO) mice. Morphological and microfluorimetric studies, respectively, demonstrated Cftr-dependent cell shrinkage and lower intracellular pH in WT enteroid epithelium in contrast to Cftr KO epithelium or WT epithelium treated with Cftr inhibitor 172. We conclude that crypt epithelium of murine enteroids exhibit Cftr expression and activity that recapitulates crypt epithelium in vivo. Enteroids provide a primary culture model that is suitable for physiological studies of regenerating crypt epithelium.
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Dudhwala, Zenab Mustansir, Paul D. Hammond, Gordon S. Howarth, and Adrian Gerard Cummins. "Intestinal stem cells promote crypt fission during postnatal growth of the small intestine." BMJ Open Gastroenterology 7, no. 1 (2020): e000388. http://dx.doi.org/10.1136/bmjgast-2020-000388.
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ObjectiveWnt-β-catenin signalling is essential for intestinal stem cells. Our aim was to investigate the relationship between intestinal stem cells and crypt fission which peaks during infancy.DesignDuodenal biopsies were obtained during endoscopy to assess the severity of reflux oesophagitis of 15 infants, children and teenagers, which would not affect the duodenum. Samples of small intestine were also obtained from rats 7–72 days of life. Crypt fission was assessed using microdissection of 100 whole crypts and recording the percentage of bifid crypts. Intestinal LGR5+ stem cells were identified by in situ hybridisation. Rats were treated with Dickkopf to block Wnt-β-catenin signalling.ResultsCrypt fission peaked during infancy before declining after 3–4 years in humans and after 21 days of life in rats. Occasional mitotic figures were seen in bifid crypts during early fission. Stem cells were elevated for a greater period during infancy and childhood in humans. Clustering of Paneth cells was present around the stem cells at the crypt base. Dickkopf reduced the number of stem cells and crypt fission to 45% and 29%, respectively, of control values, showing dependence of both crypt fission and Lgr5+ stem cells on Wnt signalling. However, Dickkopf did not decrease mitotic count per crypt, indicating a difference in signalling between stem cells and their progeny in the transit amplifying zone.ConclusionCrypt fission peaks during infancy and is dependent on intestinal stem cells. This is relatively hidden by ‘a cloak of invisibility’ due to the low proliferation of stem cells.
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Sigvardsen, Per E., Michael H. C. Pham, Jørgen T. Kühl, et al. "Left ventricular myocardial crypts: morphological patterns and prognostic implications." European Heart Journal - Cardiovascular Imaging 22, no. 1 (2020): 75–81. http://dx.doi.org/10.1093/ehjci/jeaa020.
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Abstract Aims Left ventricular (LV) myocardial crypts are considered a subtle marker of hypertrophic cardiomyopathy. However, crypts have also been observed in seemingly healthy individuals and it is unknown whether myocardial crypts are associated with adverse outcome. Methods and results Myocardial crypts were defined as invaginations traversing &gt;50% of the myocardial wall and assessed using contrast-enhanced cardiac computed tomography in 10 097 individuals from the Copenhagen General Population Study. Number of crypts, location, shape, penetrance, and volume were assessed. The endpoint was a composite of major adverse cardiovascular events and defined as death, myocardial infarction, heart failure, or stroke. Cox regression models were adjusted for clinical variables, medical history, electrocardiographic parameters, and cardiac chamber sizes. A total of 1199 LV myocardial crypts were identified in 915 (9.1%) individuals. Seven hundred (6.9%) had one crypt and 215 (2.1%) had multiple crypts. During a median follow-up of 4.0 years (interquartile range 1.5–6.7), major adverse cardiovascular events occurred in 619 individuals. Individuals with one or multiple crypts had a hazard ratio for major adverse cardiovascular events of 1.00 [95% confidence interval (CI): 0.72–1.40; P = 0.98] and 0.90 (95% CI: 0.47–1.75; P = 0.76), respectively, compared with those with no crypts. No specific pattern of crypt location, shape, penetrance, or volume was associated to an increased hazard ratio for major adverse cardiovascular events. Conclusion LV myocardial crypts are frequent in the general population and are not associated with intermediate-term major adverse cardiovascular events.
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Natoli, Valentino, Luca Viganò, and Cinzia Casu. "Cryptic Tonsils and Halitosis: An Overview of the Literature and a Clinical Image." Cross Current International Journal of Medical and Biosciences 1, no. 5 (2019): 117–21. http://dx.doi.org/10.36344/ccijmb.2019.v01i05.001.
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Cryptic tonsils are the manifestation of repeated inflammation of the tonsils. In particular, the term is used to indicate the occupation of the space of the crypts present on the surface of the tonsillar glands, by infectious debris, deposits of calcific material or food residues. Cryptic tonsils are associated with the appearance of whitish plaques (tonsillolith) and bad breath (halitosis), ear pain, sore throat, hypertrophic tonsils and swallowing problems. A 25-year-old patient comes to the practice for oral hygiene when we notice his cryptic tonsils that cause him to form tonsilloliths and halitosis, creating embarrassment for the patient and limits in interpersonal relationships.
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Waspada, Ikaputera, Dwi Fitrizal Salim, and Astrie Krisnawati. "Horizon of cryptocurrency before vs during COVID-19." Investment Management and Financial Innovations 20, no. 1 (2022): 14–25. http://dx.doi.org/10.21511/imfi.20(1).2023.02.
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Investment cannot be separated from the level of return and risk inherent in assets. Today, investment instruments are not only stocks, currencies, bonds, deposits, savings and others. The beginning of Bitcoin’s emergence as a pioneer of Cryptocurrency was in 2009. Crypto assets are emerging rapidly and are accompanied by an increase in the number of transactions each period. The growth in the market capitalization value of crypto assets has also grown significantly. During COVID-19, many investments, such as stocks, experienced a decline due to market uncertainty. The results of this study prove that with the existence of COVID-19, the crypto market is not affected. Crypto is an attraction characterized by a high degree of fluctuation, and there is no limit to transactions in the open market 24 hours to trade. The Cryptocurrency market is currently a market that can provide short-term benefits to risk-taking investors, while the market in other investment instruments is declining. 78% of the value capitalization of the top 200 cryptocurrencies is represented by the top 9 cryptos used as samples in this study. So that if there is a decrease in these 9 cryptos, it will also have an impact on the overall capitalization value of crypto in the market. The future development of Cryptocurrencies will no longer be digital assets traded with many speculators who can control prices, it can even be digital money that can be used worldwide without any transaction fees and is controlled on a blockchain system.
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Limberis, Natalia, and Ivan Marchenko. "Crypt of the Roman Times from the Barrow Necropolis of Vinogradnoe-7 Settlement on the Taman Peninsula." Stratum plus. Archaeology and Cultural Anthropology, no. 4 (August 30, 2021): 349–58. http://dx.doi.org/10.55086/sp214349358.
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The authors publish and study items from the crypt, discovered in one of the burial mounds of the necropolis located on the Phanagoria Chora. The crypt, built around the middle of the 1st century AD, was used for 50—70 years. In the early period of the crypt’s existence (mid–third quarter of the 1st century AD), 6—7 burials were made, and fully robbed later. The next one was burial III in the southern part of the chamber. This burial was also robbed in antiquity, but some of the bones and items remained in place. In the northern half of the crypt there are intact burials I and II with accompanying equipment. The inventory of the three surviving burials contains terra sigillata, glass vessels and fibulae. The chronology of these objects made it possible to limit the final stage of the crypt’s existence to the last quarter of the 1st century AD — the beginning of the 2nd century AD.
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Crispel, Yonatan, Ron Shaoul, Ranya Khamaise, Edmond Sabo, and Ze’ev Hochberg. "Effect of weaning age on the small intestine mucosa of rats." Applied Physiology, Nutrition, and Metabolism 44, no. 9 (2019): 985–89. http://dx.doi.org/10.1139/apnm-2018-0454.
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Weaning of mammalian progeny is associated with a change in food composition and mother–offspring separation. Weaning results in a critical period of low voluntary feed intake, during which the animal is adapting to the starter diet. To evaluate the effects of weaning age on morphological changes that occur in the intestines of rats, we assessed intestinal histomorphometry and somatic growth in 21-days-old pups and 90-days-old mature rats that had been weaned early (day 16), normally (day 21), or late (day 26). Early weaning resulted in deeper crypts, lower villous/crypt ratio, and a smaller villous area on day 21. Crown-tail length correlated positively with the crypt depth and negatively with the villous/crypt ratio. At age 90 days, early weaned animals had shallower crypts, a greater villous/crypt ratio, and a smaller villous area compared with their normally weaned counterparts. The rats’ crown-tail length correlated negatively with the crypt depth and positively with the villous/crypt ratio. Early weaning significantly affects the intestinal mucosa, which may impact food absorption and lead to differences in somatic growth compared with late weaning. Over time there may be a phase of compensation with increased villus height and crypt depth.
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Rajendran, Vazhaikkurichi M., Satish K. Singh, John Geibel, and Henry J. Binder. "Differential localization of colonic H+-K+-ATPase isoforms in surface and crypt cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 2 (1998): G424—G429. http://dx.doi.org/10.1152/ajpgi.1998.274.2.g424.
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Two distinct colonic H+-K+-adenosinetriphosphatase (H+-K+-ATPase) isoforms can be identified in part on the basis of their sensitivity to ouabain. The colonic H+-K+-ATPase α-subunit (HKcα) was recently cloned, and its message and protein are present in surface (and the upper 20% of crypt) cells in the rat distal colon. These studies were performed to establish the spatial distribution of the ouabain-sensitive and ouabain-insensitive components of both H+-K+-ATPase activity in apical membranes prepared from surface and crypt cells and K+-dependent intracellular pH (pHi) recovery from an acid load both in isolated perfused colonic crypts and in surface epithelial cells. Whereas H+-K+-ATPase activity in apical membranes from surface cells was 46% ouabain sensitive, its activity in crypt apical membranes was 96% ouabain sensitive. Similarly, K+-dependent pHi recovery in isolated crypts was completely ouabain sensitive, whereas in surface cells K+-dependent pHi recovery was insensitive to ouabain. These studies provide compelling evidence that HKcα encodes the colonic ouabain-insensitive H+-K+-ATPase and that a colonic ouabain-sensitive H+-K+-ATPase isoform is present in colonic crypts and remains to be cloned and identified.
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Bull, Cecilia, Dilip Malipatlolla, Marie Kalm, et al. "A novel mouse model of radiation-induced cancer survivorship diseases of the gut." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 5 (2017): G456—G466. http://dx.doi.org/10.1152/ajpgi.00113.2017.
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A deeper understanding of the radiation-induced pathophysiological processes that develop in the gut is imperative to prevent, alleviate, or eliminate cancer survivorship diseases after radiotherapy to the pelvic area. Most rodent models of high-dose gastrointestinal radiation injury are limited by high mortality. We therefore established a model that allows for the delivering of radiation in fractions at high doses while maintaining long-term survival. Adult male C57/BL6 mice were exposed to small-field irradiation, restricted to 1.5 cm of the colorectum using a linear accelerator. Each mouse received 6 or 8 Gy, two times daily in 12-h intervals in two, three, or four fractions. Acute cell death was examined at 4.5 h postirradiation and histological changes at 6 wk postirradiation. Another group was given four fractions of 8 Gy and followed over time for development of visible symptoms. Irradiation caused immediate cell death, mainly limited to the colorectum. At 6 wk postirradiation, several crypts displayed signs of radiation-induced degeneration. The degenerating crypts were seen alongside crypts that appeared perfectly healthy. Crypt survival was reduced after the fourth fraction regardless of dose, whereas the number of macrophages increased. Angiogenesis was induced, likely as a compensatory mechanism for hypoxia. Four months postirradiation, mice began to show radiation-induced symptoms, and histological examination revealed an extensive crypt loss and fibrosis. Our model is uniquely suitable for studying the long-term trajectory and underlying mechanisms of radiation-induced gastrointestinal injury. NEW & NOTEWORTHY A novel mouse model for studying the long-term trajectory of radiation-induced gut injury. The method allows for the use of high doses and multiple fractions, with minor impact on animal health for at least 3 mo. Crypt loss and a slow progression of fibrosis is observed. Crypt degeneration is a process restricted to isolated crypts. Crypt degeneration is presented as a convenient proxy endpoint for long-term radiation-induced gut injury.
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Ingham-Dempster, Tim, Dawn C. Walker, and Bernard M. Corfe. "An agent-based model of anoikis in the colon crypt displays novel emergent behaviour consistent with biological observations." Royal Society Open Science 4, no. 4 (2017): 160858. http://dx.doi.org/10.1098/rsos.160858.
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Colorectal cancer (CRC) is a major cause of cancer mortality. Colon crypts are multi-cellular flask-shaped invaginations of the colonic epithelium, with stem cells at their base which support the continual turnover of the epithelium with loss of cells by anoikis from the flat mucosa. Mutations in these stem cells can become embedded in the crypts, a process that is strongly implicated in CRC initiation. We describe a computational model which includes novel features, including an accurate representation of the geometry of the crypt mouth. Model simulations yield previously unseen emergent phenomena, such as localization of cell death to a small region of the crypt mouth which corresponds with that observed in vivo . A mechanism emerges in the model for regulation of crypt cellularity in response to changes in either cell proliferation rates or membrane adhesion strengths. We show that cell shape assumptions influence this behaviour, with cylinders recapitulating biology better than spheres. Potential applications of the model include determination of roles of mutations in neoplasia and exploring factors for altered crypt morphodynamics.
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Chu, Jingsong, Shaoyou Chu, and Marshall H. Montrose. "Apical Na+/H+ exchange near the base of mouse colonic crypts." American Journal of Physiology-Cell Physiology 283, no. 1 (2002): C358—C372. http://dx.doi.org/10.1152/ajpcell.01380.2000.
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Colonic crypts can absorb fluid, but the identity of the absorptive transporters remains speculative. Near the crypt base, the epithelial cells responsible for vectorial transport are relatively undifferentiated and often presumed to mediate only Cl−secretion. We have applied confocal microscopy in combination with an extracellular fluid marker [Lucifer yellow (LY)] or a pH-sensitive dye (2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein) to study mouse colonic crypt epithelial cells directly adjacent to the crypt base within an intact mucosal sheet. Measurements of intracellular pH report activation of colonocyte Na+/H+ exchange in response to luminal or serosal Na+. Studies with LY demonstrate the presence of a paracellular fluid flux, but luminal Na+ does not activate Na+/H+ exchange in the nonepithelial cells of the lamina propria, and studies with LY suggest that the fluid bathing colonocyte basolateral membranes is rapidly refreshed by serosal perfusates. The apical Na+/H+ exchange in crypt colonocytes is inhibited equivalently by luminal 20 μM ethylisopropylamiloride and 20 μM HOE-694 but is not inhibited by luminal 20 μM S-1611. Immunostaining reveals the presence of epitopes from NHE1 and NHE2, but not NHE3, in epithelial cells near the base of colonic crypts. Comparison of apical Na+/H+exchange activity in the presence of Cl− with that in the absence of Cl− (substitution by gluconate or nitrate) revealed no evidence of the Cl−-dependent Na+/H+ exchange that had been previously reported as the sole apical Na+/H+ exchange activity in the colonic crypt. Results suggest the presence of an apical Na+/H+ exchanger near the base of crypts with functional attributes similar to those of the cloned NHE2 isoform.
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Gurrib, Ikhlaas. "Can energy commodities affect energy blockchain-based cryptos?" Studies in Economics and Finance 36, no. 4 (2019): 682–99. http://dx.doi.org/10.1108/sef-10-2018-0313.
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Purpose The purpose of this paper is to shed fresh light into whether an energy commodity price index (ENFX) and energy blockchain-based crypto price index (ENCX) can be used to predict movements in the energy commodity and energy crypto market. Design/methodology/approach Using principal component analysis over daily data of crude oil, heating oil, natural gas and energy based cryptos, the ENFX and ENCX indices are constructed, where ENFX (ENCX) represents 94% (88%) of variability in energy commodity (energy crypto) prices. Findings Natural gas price movements were better explained by ENCX, and shared positive (negative) correlations with cryptos (crude oil and heating oil). Using a vector autoregressive model (VAR), while the 1-day lagged ENCX (ENFX) was significant in estimating current ENCX (ENFX) values, only lagged ENCX was significant in estimating current ENFX. Granger causality tests confirmed the two markets do not granger cause each other. One standard deviation shock in ENFX had a negative effect on ENCX. Weak forecasting results of the VAR model, support the two markets are not robust forecasters of each other. Robustness wise, the VAR model ranked lower than an autoregressive model, but higher than a random walk model. Research limitations/implications Significant structural breaks at distinct dates in the two markets reinforce that the two markets do not help to predict each other. The findings are limited by the existence of bubbles (December 2017-January 2018) which were witnessed in energy blockchain-based crypto markets and natural gas, but not in crude oil and heating oil. Originality/value As per the authors’ knowledge, this is the first paper to analyze the relationship between leading energy commodities and energy blockchain-based crypto markets.
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Green, S. E., P. Chapman, J. Burn, et al. "Colonic epithelial cell proliferation in hereditary non-polyposis colorectal cancer." Gut 43, no. 1 (1998): 85–92. http://dx.doi.org/10.1136/gut.43.1.85.
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Background—Despite the recent discovery of four genes responsible for up to 90% of all cases of hereditary non-polyposis colorectal cancer (HNPCC), there will still be families in whom predictive testing is not possible. A phenotypic biomarker would therefore be useful. An upwards shift of the proliferative compartment in colonic crypts is reported to be one of the earliest changes in premalignant mucosa.Aims—To assess the role of crypt cell proliferation as a phenotypic biomarker in HNPCC.Patients—Thirty five patients at 50% risk of carrying the HNPCC gene (21 of whom subsequently underwent predictive testing and hence gene carrier status was known) and 18 controls.Methods—Crypt cell proliferation was measured at five sites in the colon using two different techniques. Labelling index was determined using the monoclonal antibody MIB1 and whole crypt mitotic index was measured using the microdissection and crypt squash technique. The distribution of proliferating cells within the crypts was also assessed.Results—There were no significant differences in the total labelling index or mean number of mitoses per crypt, nor in the distribution of proliferating cells within the crypt, between the study and control groups at any site. When the 21 patients in whom gene carrier status was known were analysed separately there were no significant differences in the measured indices of proliferation between the HNPCC gene carriers and non-gene carriers.Conclusion—Crypt cell proliferation is not a discriminative marker of gene carriage in HNPCC.
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George, Robert J., Mark A. Sturmoski, Randal May, et al. "Loss of p21Waf1/Cip1/Sdi1enhances intestinal stem cell survival following radiation injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 2 (2009): G245—G254. http://dx.doi.org/10.1152/ajpgi.00021.2008.
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The microcolony assay following gamma irradiation (IR) is a functional assay of intestinal stem cell fate. The cyclin-dependent kinase (CDK) inhibitor p21Waf1/Cip1/Sdi1(p21) regulates cell cycle arrest following DNA damage. To explore the role of p21 on stem cell fate, we examined the effects of p21 deletion on intestinal crypt survival following IR and expression of the stem/progenitor cell marker Musashi-1 (Msi-1) and the antiapoptotic gene survivin. Intestinal stem cell survival in adult wild-type (WT) and p21−/−mice was measured using the microcolony assay. Msi-1, p21, and survivin mRNA were measured using real-time PCR and immunohistochemical analysis. Laser capture microdissection (LCM) was used to isolate mRNA from the crypt stem cell zone. No differences in radiation-induced apoptosis were observed between WT and p21−/−mice. However, increased crypt survival (3.0-fold) was observed in p21−/−compared with WT mice 3.5 days after 13 Gy. Msi-1 and survivin mRNA were elevated 12- and 7.5-fold, respectively, in LCM-dissected crypts of p21−/−compared with WT mice. In conclusion, deletion of p21 results in protection of crypt stem/progenitor cells from IR-induced cell death. Furthermore, the increase in crypt survival is associated with increased numbers of Msi-1- and survivin-expressing cells in regenerative crypts.
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Walrath, Travis, Robert A. Malizia, Xinjun Zhu та ін. "IFN-γ and IL-17A regulate intestinal crypt production of CXCL10 in the healthy and inflamed colon". American Journal of Physiology-Gastrointestinal and Liver Physiology 318, № 3 (2020): G479—G489. http://dx.doi.org/10.1152/ajpgi.00208.2019.
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During intestinal inflammation, immature cells within the intestinal crypt are called upon to replenish lost epithelial cell populations, promote tissue regeneration, and restore barrier integrity. Inflammatory mediators including TH1/TH17-associated cytokines influence tissue health and regenerative processes, yet how these cytokines directly influence the colon crypt epithelium and whether the crypt remains responsive to these cytokines during active damage and repair, remain unclear. Here, using laser-capture microdissection and primary colon organoid culture, we show that the cytokine milieu regulates the ability of the colonic crypt epithelium to participate in proinflammatory signaling. IFN-γ induces the TH1-recruiting, proinflammatory chemokine CXCL10/IP10 in primary murine intestinal crypt epithelium. CXCL10 was also induced in colonic organoids derived from mice with active, experimentally induced colitis, suggesting that the crypt can actively secrete CXCL10 in select cytokine environments during colitis. Colon expression of cxcl10 further increased during infectious and noninfectious colitis in Il17a−/− mice, demonstrating that IL-17A exerts a negative effect on CXCL10 in vivo. Furthermore, IL-17A directly antagonized CXCL10 production in ex vivo organoid cultures derived from healthy murine colons. Interestingly, direct antagonism of CXCL10 was not observed in organoids derived from colitic mouse colons bearing active lesions. These data, highlighting the complex interplay between the cytokine milieu and crypt epithelia, demonstrate proinflammatory chemokines can be induced within the colonic crypt and suggest the crypt remains responsive to cytokine modulation during inflammation. NEW & NOTEWORTHY Upon damage, the intestinal epithelium regenerates to restore barrier function. Here we observe that the local colonic cytokine milieu controls the production of procolitic chemokines within the crypt base and colon crypts remain responsive to cytokines during inflammation. IFN-γ promotes, while IL-17 antagonizes, CXCL10 production in healthy colonic crypts, while responses to cytokines differ in inflamed colon epithelium. These data reveal novel insight into colon crypt responses and inflammation-relevant alterations in signaling.
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McCullough, J. S., B. Ratcliffe, N. Mandir, K. E. Carr, and R. A. Goodlad. "Dietary fibre and intestinal microflora: effects on intestinal morphometry and crypt branching." Gut 42, no. 6 (1998): 799–806. http://dx.doi.org/10.1136/gut.42.6.799.
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Background—Fermentable dietary fibre has many effects on the gastrointestinal tract. One is to alter epithelial crypt cell proliferation, especially in the colon. A discrepancy between epithelial cell production rates and intestinal weights has been noted previously: crypt cell production rates only increase if bacterial fermentation occurs, but intestinal wet weight can increase in the same animals without bacterial fermentation of fibre.Aims—To quantify intestinal cell populations in order to resolve the above paradox.Methods—Conventional and germ-free rats were fed fibre-free or fibre supplemented diets and their intestines were quantified by morphometry.Results—There was evidence of fibre associated muscle hypertrophy in the colon, but the main effect of fibre was an increase in the number of crypts per circumference and also the number of branched crypts in the proximal colon in both groups. There was also a large increase in the number of branched crypts in the mid colon of the germ-free rats (both fibre-free and fibre supplemented). Fibre had a direct (bacteria independent) effect on goblet cells in the small intestine and a direct effect on the goblet cells in the colon, which was attenuated by the presence of bacteria. There was a notable decline in the number of enteroendocrine cells in the small intestine of the germ-free animals.Conclusions—Fibre has several direct and indirect effects on the gut. In the proximal colon it can directly increase the number of crypts present. This provides a means for increasing intestinal mass in addition to intestinal crypt cell production.
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Poindexter, Shenika V., Vishruth K. Reddy, Mukul K. Mittal, et al. "Transcriptional corepressor MTG16 regulates small intestinal crypt proliferation and crypt regeneration after radiation-induced injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 6 (2015): G562—G571. http://dx.doi.org/10.1152/ajpgi.00253.2014.
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Myeloid translocation genes (MTGs) are transcriptional corepressors implicated in development, malignancy, differentiation, and stem cell function. While MTG16 loss renders mice sensitive to chemical colitis, the role of MTG16 in the small intestine is unknown. Histological examination revealed that Mtg16 −/− mice have increased enterocyte proliferation and goblet cell deficiency. After exposure to radiation, Mtg16 −/− mice exhibited increased crypt viability and decreased apoptosis compared with wild-type (WT) mice. Flow cytometric and immunofluorescence analysis of intestinal epithelial cells for phospho-histone H2A.X also indicated decreased DNA damage and apoptosis in Mtg16 −/− intestines. To determine if Mtg16 deletion affected epithelial cells in a cell-autonomous fashion, intestinal crypts were isolated from Mtg16 −/− mice. Mtg16 −/− and WT intestinal crypts showed similar enterosphere forming efficiencies when cultured in the presence of EGF, Noggin, and R-spondin. However, when Mtg16 −/− crypts were cultured in the presence of Wnt3a, they demonstrated higher enterosphere forming efficiencies and delayed progression to mature enteroids. Mtg16 −/− intestinal crypts isolated from irradiated mice exhibited increased survival compared with WT intestinal crypts. Interestingly, Mtg16 expression was reduced in a stem cell-enriched population at the time of crypt regeneration. This is consistent with MTG16 negatively regulating regeneration in vivo. Taken together, our data demonstrate that MTG16 loss promotes radioresistance and impacts intestinal stem cell function, possibly due to shifting cellular response away from DNA damage-induced apoptosis and towards DNA repair after injury.
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Mahler, Robert, Włodzimierz Godlewski, Katarzyna Danys-Lasek, and Barbara Czaja. "Crypt 3 in the Northwest Annex of the Monastery on Kom H in Dongola: report on the exploration in 2012." Polish Archaeology in the Mediterranean XXIV, no. 1 (2016): 352–67. http://dx.doi.org/10.5604/01.3001.0010.0032.
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Archaeological exploration of Crypt 3 in the commemorative burial complex in the Northwest Annex of the Monastery on Kom H in Dongola in 2012 completed the process of investigation of the three crypts, discovered in the mid-1990s but not fully excavated at the time. Crypt 3, built together with Crypt 2, hosted remains of five individuals. Remains of textiles and grave furnishings were also discovered, among them an oil lamp and part of a broken amphora. Crypt 3 constituted an integral part of a commemorative complex consisting of a naos, two sanctuaries with altars and screens, and a prothesis with altar.
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Traber, P. G., W. Wang, and L. Yu. "Differential regulation of cytochrome P-450 genes along rat intestinal crypt-villus axis." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 2 (1992): G215—G223. http://dx.doi.org/10.1152/ajpgi.1992.263.2.g215.
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Mammalian small intestine contains cytochrome P-450-dependent monooxygenase enzymes that are capable of metabolizing a wide variety of xenobiotics and activating procarcinogens to mutagenic compounds. The epithelial cells lining the small intestine are separated into a proliferating undifferentiated compartment located in crypts and a nonproliferating differentiated compartment located on villi. The constitutive expression and induction by xenobiotics of genes that encode components of the cytochrome P-450-dependent mono-oxygenase system along the rat intestinal crypt-villus axis were investigated using isolated epithelial cells and in situ hybridization. For each gene examined, hybridization analysis of RNA obtained from isolated epithelial cells correlated with findings on in situ RNA hybridization. Cytochrome P-450IA1 mRNA (CYP1A1), the major aromatic hydrocarbon-inducible P-450, and cytochrome P-450IIB1 mRNA (CYP2B1), the major phenobarbital-inducible P-450, were constitutively expressed in villus cells with no detectable mRNA present in crypts. Treatment with several chemical inducers resulted in a marked increase in CYP1A1 mRNA in both crypt and villus cells. In contrast, although CYP2B1 mRNA was inducible in villus cells, CYP2B1 mRNA was not detected in crypts after treatment with chemical inducers. NADPH cytochrome P-450 reductase, a necessary component for the activity of all P-450 enzymes, was expressed constitutively at low levels only in villus cells. Treatment with dexamethasone induced reductase mRNA in both crypt and villus cells. Taken together, these results demonstrate that there is a complex gene-specific pattern of expression of the microsomal monooxygenase system along the crypt-villus axis of rat small intestine.(ABSTRACT TRUNCATED AT 250 WORDS)
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Yates, Catherine A., Gareth S. Evans, and Hilary J. Powers. "Riboflavin deficiency: early effects on post-weaning development of the duodenum in rats." British Journal of Nutrition 86, no. 5 (2001): 593–99. http://dx.doi.org/10.1079/bjn2001420.
Full textAbstract:
The aim of this present study was to identify the earliest point at which riboflavin deficiency affects post-weaning bowel development in rats. After weaning, eighty Wistar rats were weight-matched as pairs, one animal being fed a normal synthetic diet and the other being fed the same diet but deficient in riboflavin. Body weight, feeding and rates of growth were monitored and eight pairs of animals were taken for analysis at 45, 69, 93, 117 and 141 h. Riboflavin status was monitored by determining the erythrocyte glutathione reductase activation coefficient (EGRAC), and hepatic flavins were measured by a fluorescence assay. Changes to the number and dimensions of villi and crypts in the duodenum were determined, as well as crypt division (bifurcation) and the DNA synthesis index of the crypt epithelium by bromodeoxyuridine (BrdU) labelling. Riboflavin deficiency was established in the experimental rats, as demonstrated by a significant increase in EGRAC after 45 h (P<0·001) and decreased liver flavins after 96 h (P<0·001). After 96 h a significant increase in the size and cellularity of the crypts (P<0·001 in both cases) was seen in these riboflavin-deficient animals, with a decreased incidence of bifurcating crypts and of BrdU-labelled cells. No changes to villus number or size were observed. The present study has demonstrated that developmental changes to the duodenal crypt arise shortly after circulating riboflavin measurements show evidence of deficiency. These changes primarily affect cell proliferation and crypt bifurcation, and precede long-term changes such as the reduction of villus number.
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Sei, Yoshitatsu, Xinping Lu, Alice Liou, Xilin Zhao, and Stephen A. Wank. "A stem cell marker-expressing subset of enteroendocrine cells resides at the crypt base in the small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 2 (2011): G345—G356. http://dx.doi.org/10.1152/ajpgi.00278.2010.
Full textAbstract:
The spatial orientation of the enteroendocrine cells along the crypt-villus axis is closely associated with their differentiation in the intestine. Here we studied this relationship using primary duodenal crypts and an ex vivo organoid system established from cholecystokinin-green fluorescent protein (CCK-GFP) transgenic mice. In the primary duodenal crypts, GFP+ cells were found not only in the upper crypt but also at the crypt base, where the stem cells reside. Many GFP+ cells below +4 position were positive for the putative intestinal stem cell markers, leucine-rich repeat-containing G protein-coupled receptor 5, CD133, and doublecortin and CaM kinase-like-1, and also for the neuroendocrine transcription factor neurogenin 3. However, these cells were neither stem nor transient amplifying precursor cells because they were negative for both Ki-67 and phospho-Histone H3 and positive for the mature endocrine marker chromogranin A. Furthermore, these cells expressed multiple endocrine hormones. Tracking of GFP+ cells in the organoids from CCK-GFP mice indicated that GFP+ cells were first observed around the +4 position, some of which localized to the crypt base later in the culture period. These results suggest that a subset of enteroendocrine cells migrates down to the crypt base or stays localized at the crypt base, where they express stem and postmitotic endocrine markers. Further investigation of the function of this subset may provide novel insights into the genesis and development of enteroendocrine cells as well as enteroendocrine tumorigenesis.
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Yuan, Jia, Jeeyeon Cha, Wenbo Deng, et al. "Planar cell polarity signaling in the uterus directs appropriate positioning of the crypt for embryo implantation." Proceedings of the National Academy of Sciences 113, no. 50 (2016): E8079—E8088. http://dx.doi.org/10.1073/pnas.1614946113.
Full textAbstract:
Blastocyst implantation is a complex process requiring coordination of a dynamic sequence of embryo–uterine interactions. Blood vessels enter the uterus from the mesometrium, demarcating the uterus into mesometrial (M) and antimesometrial (AM) domains. Implantation occurs along the uterine longitudinal axis within specialized implantation chambers (crypts) that originate within the evaginations directed from the primary lumen toward the AM domain. The morphological orientation of crypts in rodent uteri was recognized more than a century ago, but the mechanism remained unknown. Here we provide evidence that planar cell polarity (PCP) signaling orchestrates directed epithelial evaginations to form crypts for implantation in mice. Uterine deletion of Vang-like protein 2, but not Vang-like protein 1, conferred aberrant PCP signaling, misdirected epithelial evaginations, defective crypt formation, and blastocyst attachment, leading to severely compromised pregnancy outcomes. The study reveals a previously unrecognized role for PCP in executing spatial cues for crypt formation and implantation. Because PCP is an evolutionarily conserved phenomenon, our study is likely to inspire implantation studies of this signaling pathway in humans and other species.
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Wilkins, Heather R., Kinuko Ohneda, Temitope O. Keku, et al. "Reduction of spontaneous and irradiation-induced apoptosis in small intestine of IGF-I transgenic mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 2 (2002): G457—G464. http://dx.doi.org/10.1152/ajpgi.00019.2002.
Full textAbstract:
Insulin-like growth factor I (IGF-I) may promote survival of putative stem cells in the small intestinal epithelium. Mitosis and apoptosis were quantified in crypts of nonirradiated and irradiated IGF-I transgenic (TG) and wild-type (WT) littermates. The mean apoptotic index was significantly greater in WT vs. TG littermates. After irradiation, apoptotic indexes increased, and WT mice showed a more dramatic increase in apoptosis than TG mice at the location of putative stem cells. After irradiation, no mitotic figures were observed in WT crypts, whereas mitosis was maintained within the jejunal epithelium of TG mice. The abundance and localization of Bax mRNA did not differ between nonirradiated littermates. However, there was more Bax mRNA in TG vs. WT mice after irradiation. Bax mRNA was located along the entire length of the irradiated crypt epithelium, but there was less Bax protein observed in the bottom third of TG mouse crypts compared with WT littermates. IGF-I regulates cell number by stimulating crypt cell proliferation and decreasing apoptosis preferentially within the stem cell compartment.
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Paulsen, Jan Erik, Else Marit Løberg, Hege Benedikte Ølstørn, Helle Knutsen, Inger-Lise Steffensen, and Jan Alexander. "Flat Dysplastic Aberrant Crypt Foci Are Related to Tumorigenesis in the Colon of Azoxymethane-Treated Rat." Cancer Research 65, no. 1 (2005): 121–29. http://dx.doi.org/10.1158/0008-5472.121.65.1.
Full textAbstract:
Abstract We evaluated the role of aberrant crypt foci (ACF) as biomarkers of colon cancer by studying the sequential development (6-28 weeks) from early lesion to tumor in the colon of azoxymethane-exposed F344 rats (15 mg/kg bw × 2). Surface examination of unsectioned methylene blue–stained colon preparations, transilluminated in the inverse light microscope, revealed two types of early lesions: classic elevated ACF and small flat lesions, which we denoted flat ACF and which were characterized by bright blue staining, compressed crypt openings, and crypts not elevated above the surrounding mucosa. At a later stage, the crypts surrounding large flat ACF became enlarged, a change that slightly raised the structure; principally, large flat ACF and nascent tumors displayed the same surface morphology. Furthermore, flat ACF with 18.6 ± 10.6 crypt/focus and tumors showed a uniform picture of severe dysplasia with frequent presence of Paneth cells, compressed crypts, cytoplasmic/nuclear overexpression of β-catenin, and nuclear overexpression of cyclin D1. In contrast, classic elevated ACF with 5.3 ± 2.5 crypts/focus did not display such changes: they showed mainly hyperplasia, mild or moderate dysplasia but never severe dysplasia. Along the time course, the number of flat ACF + tumors, including microscopic and macroscopic, was virtually constant, ∼2.5 lesions/rat. The number of classic elevated ACF was initially ∼180 lesions/rat and terminally ∼80 lesions/rat. Flat ACF grew significantly faster than classic elevated ACF. In conclusion, our data indicate a continuous developmental growth from small flat dysplastic ACF to the stage of a tumor. In contrast, classic elevated ACF do not seem to be as closely related to tumorigenesis.
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Kockerling, A., D. Sorgenfrei, and M. Fromm. "Electrogenic Na+ absorption of rat distal colon is confined to surface epithelium: a voltage-scanning study." American Journal of Physiology-Cell Physiology 264, no. 5 (1993): C1285—C1293. http://dx.doi.org/10.1152/ajpcell.1993.264.5.c1285.
Full textAbstract:
There is no quantitative assignment of large intestinal electrogenic Na+ absorption to surface epithelium and crypts so far. We determined the spatial distribution of electrogenic Na+ absorption to crypts and surface epithelium of rat late distal colon using a modified voltage-scanning technique. Voltage deflections resulting from external 30-Hz current were sensed by an extracellular microelectrode stepping at 0.7 Hz above crypt openings or surface epithelium. Local conductances were calculated applying a planar model of electrical field distribution to surface epithelium and a electrostatic disk source model to the crypts. These models were confirmed by methodological experiments where the electrode position was varied in vertical and horizontal direction. Electrogenic Na+ absorption was detected by blocking apical Na+ channels by mucosal 0.1 mM amiloride. Under control conditions surface epithelium contributed 44% (2.0 +/- 0.2 mS/cm2) and crypts 56% (2.6 +/- 0.2 mS/cm2) to the total conductance of 4.6 +/- 0.4 mS/cm2. Electrogenic Na+ absorption was induced by 6 h in vitro incubation in a medium containing 3 nM aldosterone. This caused a short-circuit current (ISC) of 12.1 +/- 0.8 mumol.h-1.cm-2, which was paralleled by a 2.5-fold increase in surface epithelial conductance to 5.1 +/- 0.4 mS/cm2, whereas crypt conductance was not significantly altered (3.0 +/- 0.2 mS/cm2). Amiloride reversed ISC to -0.8 +/- 0.1 mumol.-1.cm-2 and decreased surface epithelium conductance to 2.3 +/- 0.3 mS/cm2 but again had no significant effect on crypt conductance (2.5 +/- 0.3 mS/cm2). Sham incubation (no hormones added) for 6 h neither induced electrogenic transport nor altered local epithelial conductances.(ABSTRACT TRUNCATED AT 250 WORDS)
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OPANASYUK, Vitaly. "DEVELOPMENT OF UKRAINIAN CRYPTO INDUSTRY: FROM PRACTICAL EXPERIENCE TO DIGITAL LEADERSHIP." Herald of Khmelnytskyi National University 302, no. 1 (2022): 209–14. http://dx.doi.org/10.31891/2307-5740-2022-302-1-35.
Full textAbstract:
The urgency of the problem. The urgency of this topic is dictated by the strengthening of the global crypto lobby and the involvement of large and system capital in the crypto industry. Ignoring this fact can mean losing the investment race before it starts. High mobility and unlimited capacity of the crypto industry can be a good chance for Ukraine to know its niche in global cooperation. Methods: methodological and informational basis of the work are: scientific works, materials of periodicals, internet resources, normative-legal acts. In the course of the research are methods of structural-logical analysis, comparison and generalization were used. Results: A number of tax and economic incentives for the development of cryptographic investment are proposed. Directions of development in specialization and cooperation of Ukraine in the world crypt industry are offered. Scientific novelty: firstly identified and proposed the perspective, place and specialization of Ukraine in the interstate cooperation from the crypt industry point of view. Practical significance: The urgency of the topic is determined by the specialization and cooperation of Ukraine in the world of crypt industry and all significant opportunities that this young industry opens. In addition, the willingness of private investors to take higher risks, comparing with classic investments, makes Ukraine one of the few areas that concentrates both unprofessional and professional investors. That fact gives some benefits to the starting crypt industry development. First of them- to go through the formation of an expert layer,second- to form a group of professional investors and the third one- to explore the impact of cryptographic investment on GDP and competitiveness index.
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Samuel, S., R. Walsh, J. Webb, A. Robins, C. Potten, and Y. R. Mahida. "Characterization of putative stem cells in isolated human colonic crypt epithelial cells and their interactions with myofibroblasts." American Journal of Physiology-Cell Physiology 296, no. 2 (2009): C296—C305. http://dx.doi.org/10.1152/ajpcell.00383.2008.
Full textAbstract:
Colonic epithelial stem cells are believed to be located at the crypt base where they have previously been shown to express musashi-1. The colonic stem cell niche, which includes extracellular matrix and myofibroblasts (together with other cell types), is likely to be important in maintaining the function of the progenitor cells. The aims of our studies were to characterize stem cells in isolated and disaggregated human colonic crypt epithelial cells and investigate their interactions with monolayers of primary human colonic myofibroblasts. In unfractionated preparations of disaggregated colonic crypts, musashi-1 positive cells preferentially adhered to colonic myofibroblasts, despite the presence of excess blocking anti-β1-integrin antibody. These adherent epithelial cells remained viable for a number of days and developed slender processes. Cells with side population characteristics (as demonstrated by ability to expel the dye Hoechst 33342) were consistently seen in the isolated colonic crypt epithelial cells. These side population cells expressed musashi-1, β1-integrin, BerEP4, and CD133. Sorted side population crypt epithelial cells also rapidly adhered to primary colonic myofibroblasts. In conclusion, in preparation of isolated and disaggregated human colonic crypts, cells with stem cell characteristics preferentially adhere to primary human colonic myofibroblasts in a β1-integrin-independent fashion.
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Quaroni, A. "Crypt cell development in newborn rat small intestine." Journal of Cell Biology 100, no. 5 (1985): 1601–10. http://dx.doi.org/10.1083/jcb.100.5.1601.
Full textAbstract:
Three monoclonal antibodies were prepared against luminal membranes from small intestinal cells of 3-d-old rats (YBB 1/27, YBB 3/10) and crypt cell membranes from adult rats (CC 4/80). The antibodies were shown to define specific stages of development of the intestinal crypt cells. The YBB 1/27 antigen was first detected at the luminal membrane of the epithelial cells in fetal intestine at day 20 of gestation; it was confined to the crypt cells and lower villus cells between 1 and 20-22 d after birth, and could not be detected in any region of the intestine in older animals. The YBB 3/10 antigen, identified as a set of high Mr proteins, was localized over the entire surface membrane of fetal intestinal cells and of crypt and villus cells after birth; after weaning (20-22 d after birth) it gradually disappeared from the villus cells and became confined to the region of the crypts. The CC 4/80 antigen, identified as a protein (or a set of related proteins) of molecular mass 28-34 kD, was shown to appear in the crypt cells 10-14 d after birth. Its distribution changed after weaning, when it disappeared from the crypts, and was localized in the absorptive lower villus cells. This change in pattern could, in part, be prematurely elicited by cortisone injection in younger animals. These results have demonstrated the presence of specific surface membrane components on the intestinal crypt cells, and suggested that fetal antigens may be retained in these cells after birth.
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Ahmed, Ishfaq, Badal Roy, Parthasarathy Chandrakesan та ін. "Evidence of functional cross talk between the Notch and NF-κB pathways in nonneoplastic hyperproliferating colonic epithelium". American Journal of Physiology-Gastrointestinal and Liver Physiology 304, № 4 (2013): G356—G370. http://dx.doi.org/10.1152/ajpgi.00372.2012.
Full textAbstract:
The Notch and NF-κB signaling pathways regulate stem cell function and inflammation in the gut, respectively. We investigate whether a functional cross talk exists between the two pathways during transmissible murine colonic hyperplasia (TMCH) caused by Citrobacter rodentium (CR). During TMCH, NF-κB activity and subunit phosphorylation in colonic crypts of NIH Swiss mice at days 6 and 12 were associated with increases in downstream target CXC chemokine ligand (CXCL)-1/keratinocyte-derived chemokine (KC) expression. Blocking Notch signaling acutely for 5 days with the Notch blocker dibenzazepine (DBZ) failed to inhibit crypt NF-κB activity or CXCL-1/KC expression. Chronic DBZ administration for 10 days, however, blocked Notch and NF-κB signaling in the crypts and abrogated hyperplasia. Intriguingly, chronic Notch inhibition was associated with significant increases in IL-1α, granulocyte colony-stimulating factor, monocyte chemoattractant protein 1, macrophage inflammatory protein 2, and KC in the crypt-denuded lamina propria or whole distal colon, with concomitant increases in myeloperoxidase activity. In core-3−/−mice, which are defective in intestinal mucin, DBZ administration replicated the results of NIH Swiss mice; in ApcMin/+mice, which are associated with CR-induced elevation of NF-κB-p65276expression, DBZ reversed the increase in NF-κB-p65276, which may have blocked rapid proliferation of the mutated crypts. DBZ further blocked reporter activities involving the NF-κB-luciferase reporter plasmid or the Toll-like receptor 4/NF-κB/SEAPorter HEK-293 reporter cell line, while ectopic expression of Notch-NICDreversed the inhibitory effect. Dietary bael ( Aegle marmelos ) extract (4%) and curcumin (4%) restored Notch and NF-κB cross talk in NIH Swiss mice, inhibited CR/DBZ-induced apoptosis in the crypts, and promoted crypt regeneration. Thus functional cross talk between the Notch and NF-κB pathways during TMCH regulates hyperplasia and/or inflammation in response to CR infection.