Magnetically-guided capsule panendoscopy for gastrointestinal tumors (MagCam study)
Ontology highlight
ABSTRACT:
DISEASE(S): Carcinoma Of Esophagus,gastric Tumor,large Intestine Tumor
PROVIDER: 2615098 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Colorectal cancer (CRC) screening program can reduce colon cancer-related mortality. Current CRC screening methods include stool occult blood and DNA testing, blood based tests and radiologic tests. Colonoscopy is considered the gold standard to detect colorectal neoplasms. Previous studies have estimated that cancer mortality to be 68% to 88% lower among persons who undergo screening colonoscopy than among those who do not. However, colonoscopy is an invasive examination, and 10% to 20% of patients fail to tolerate the procedure; therefore, greatly reduces the success rate of completion of colon examination.
External controllability of capsule endoscope by means of an applied magnetic field is a possible solution to the maneuvering problem. However, there is no effective system with straight forward clinical applicability till now. This is ascribable to a lack of reliable magnetic instrumentation suitable for such a purpose. We have reported that magnetic field navigator (MFN) can effectively control the locomotion of capsule endoscope. We have demonstrated the feasibility and safety of magnetic-assisted capsule endoscope for the examination of upper gastrointestinal tract. In this study, we develop a magnetic-assisted capsule colonoscope by combination of the integrated circuit complementary metal-oxide-semiconductor imaging sensor, light-emitting diode, and magnetic control technology. This magnetic-assisted capsule colonoscope operation system includes a MFN Platform, high-end hand-controlled joystick, combined circuit component, control interface and software. This magnetic-assisted capsule colonoscope operation system creates a friendly operating environment for the operators, and may establishe a novel screening system for the colon.
| 2402674 | ecrin-mdr-crc
Project description:Intervention type:DEVICE. Intervention1:Comparative study between capsule endoscopy and conventional endoscopy on the accuracy and acceptability of gastrointestinal screening, Dose form:DEVICE, Route of administration:ORAL, intended dose regimen:Preparation before and after(booster) ingesting a capsule endoscope, Lubiprostone intake after passing stomach. Control intervention1:Conventional endoscopic findings before or after capsule endoscopy, Dose form:DEVICE, Route of administration:ORAL, Intended dose regimen:Preparation before and after(booster) ingesting a capsule endoscope.
Primary outcome(s): Sensitivity and specificity. Timepoint:After acquiring data from 40 subjects.
| 2612263 | ecrin-mdr-crc
Project description:Intervention type:DEVICE
Name of intervention:Comparative study between capsule endoscopy and conventional endoscopy on the accuracy and acceptability of gastrointestinal screening
Dose form / Japanese Medical Device Nomenclature:DEVICE
Capsule endoscopy
Route of administration / Site of application:ORAL
Dose per administration:1
1
1/unit
Dosing frequency / Frequency of use:ONCE
ONCE/Examination
Planned duration of intervention:8 hours (after ingesting a capsule endoscope)
Intended dose regimen:Preparation before and after(booster) ingesting a capsule endoscope, Lubiprostone intake after passing stomach
detailes of teratment arms:Volunteers or digestive disease patients who underwent or will undergo upper and lower conventional endoscopy before or after a capsule endoscopy
Comparative intervention name:Conventional endoscopic findings before or after capsule endoscopy
Dose form / Japanese Medical Device Nomenclature:DEVICE
Capsule endoscopy
Route of administration / Site of application:ORAL
Dose per administration:1
1
1/unit
Dosing frequency / Frequency of use:ONCE
ONCE
Planned duration of intervention:Eight hours after ingesting a capsule endoscope
Intended dose regimen:Preparation before and after(booster) ingesting a capsule endoscope
Primary outcome(s): Sensitivity and specificity
Study Design: Single blind no-randomized trial, uncontrolled control, No, single blind, CONFIRMATORY
| 98701 | ecrin-mdr-crc
Project description:Cryptococcus neoformans causes meningoencephalitis and is an increasing human health threat. C. neoformans is neurotropic, and persists in the cerebrospinal fluid (CSF) of the mammalian host during infection. In order to survive in the host, pathogenic fungi must procure nutrients such as carbon and nitrogen. To enhance our understanding of nutrient acquisition during infection by Cryptococcus species, we examined utilization of nitrogen sources available in CSF. We screened for growth and capsule production of 817 global environmental and clinical isolates on various sources of nitrogen. Capsule production was assessed using ammonium and urea in the presence or absence of benomyl to determine the relationship of urea exposure to capsule production. Since urea is metabolized to ammonia and CO2 (a known signal for capsule induction), we examined urea metabolism mutants for their response to urea regarding capsule production. Non-preferred nitrogen sources were found to greatly affect capsule production in pathogenic species of Cryptococcus. Urea induced the greatest magnitude of capsule production. Capsule induction by urea was greater in Cryptococcus gattii strains than in C. neoformans strains. In addition, both environmental and clinical strains grew robustly on uric acid, casamino acids, creatinine, and asparagine as sole nitrogen sources. While substantial growth on nitrate was not apparent at day 3, growth was apparent by day 6 for all serotypes.
2013-09-25 | GSE46829 | GEO
Project description:Cryptococcus neoformans causes meningoencephalitis and is an increasing human health threat. C. neoformans is neurotropic, and persists in the cerebrospinal fluid (CSF) of the mammalian host during infection. In order to survive in the host, pathogenic fungi must procure nutrients such as carbon and nitrogen. To enhance our understanding of nutrient acquisition during infection by Cryptococcus species, we examined utilization of nitrogen sources available in CSF. We screened for growth and capsule production of 817 global environmental and clinical isolates on various sources of nitrogen. Capsule production was assessed using ammonium and urea in the presence or absence of benomyl to determine the relationship of urea exposure to capsule production. Since urea is metabolized to ammonia and CO2 (a known signal for capsule induction), we examined urea metabolism mutants for their response to urea regarding capsule production. Non-preferred nitrogen sources were found to greatly affect capsule production in pathogenic species of Cryptococcus. Urea induced the greatest magnitude of capsule production. Capsule induction by urea was greater in Cryptococcus gattii strains than in C. neoformans strains. In addition, both environmental and clinical strains grew robustly on uric acid, casamino acids, creatinine, and asparagine as sole nitrogen sources. While substantial growth on nitrate was not apparent at day 3, growth was apparent by day 6 for all serotypes. In this study, transcription profiles of urea pathway mutants (ure1 and amt1/2) and WT Cryptococcus neoformans strains were compared in a dye-swap experiment following 1hr exposure to proline or proline + urea (.25g/L).
2013-09-25 | E-GEOD-46829 | biostudies-arrayexpress
Project description:Cryptococcus neoformans is an opportunistic basidiomycete pathogen that is a major etiological agent of fungal meningoencephalitis leading to more than 180,000 deaths worldwide annually. For this pathogen, the polysaccharide capsule is a key virulence factor, which interferes with the phagocytosis by host innate immune cells, but its complex signaling networks remain elusive. In this study, we systematically analyzed capsule biosynthesis and signaling networks by using C. neoformans transcription factor (TF) and kinase mutant libraries under diverse capsule-inducing conditions, such as Dulbecco’s Modified Eagle’s (DME), Littman’s medium (LIT) and fetal bovine serum (FBS) medium. We found that deletion of GAT201, YAP1, BZP4, and ADA2 consistently causes capsule production defects in all tested media, indicating that they are capsule-regulating core TFs. Epistatic and expression analysis showed that Yap1 and Ada2 control Gat201 upstream, whereas Bzp4 and Gat201 regulate capsule production independently. We next searched for potential upstream kinases and found that mutants deleted of PKA1, BUD32, POS5, IRE1 or CDC2801 showed reduced capsule production under all three capsule induction conditions, whereas mutants deleted of HOG1 and IRK5 displayed enhanced capsule production. Notably, Pka1 and Irk5 controls induction of GAT201 and BZP4, respectively, under capsule induction condition. Finally, we monitored transcriptome profiles governed by Bzp4, Gat201, and Ada2 under capsule-inducing condition and demonstrated that these TFs regulate redundant and unique sets of downstream target genes. In conclusion, this study provides further insight into the complex regulatory mechanism of capsule production related signaling pathways in C. neoformans.
2022-10-18 | GSE208163 | GEO
Project description:Purpose: Key steps in understanding a biological process include identifying genes that are involved and determining how they are regulated. We developed a novel method for identifying TFs involved in a specific process and used it to map regulation of the key virulence factor of Cryptococcus neoformans, its capsule. Results: The map, built from expression profiles of 41 TF mutants, includes 20 TFs not previously known to regulate virulence attributes. It also reveals a hierarchy comprising executive, mid-level, and “foreman” TFs. When grouped by temporal expression pattern, these TFs explain much of the transcriptional dynamics of capsule induction. Phenotypic analysis of 41 TF deletion mutants revealed complex relationships among virulence factors and virulence in mice. Conclusions: These data resources and analyses provide the first integrated, systems level view of capsule regulation and biosynthesis. Our methods dramatically improve the efficiency with which transcriptional networks can be analyzed, making genomic approaches accessible to labs focused on specific physiological processes. A total of 288 expression profiles were generated by RNA-Seq analysis of Mutant and wildtype cells grown in capsule inducing conditions for 90 minutes. In addition, 3 replicate expression profiles were generated for wildtype cells grown in : a capsule non-inducing condition, a capsule inducing condition for 180 minutes, a capsule inducing condition for 480 minutes, and a capsule inducing condition for 1440 minutes. In addition, ChIP-seq of NRG1(CNAG_05222) in capsule inducing conditions, and USV101(CNAG_05420) in both capsule inducing and non-inducing conditions were generated.
2015-01-14 | E-GEOD-60398 | biostudies-arrayexpress
Project description:Rapidly growing antibiotic resistance among gastrointestinal pathogens, and the ability of antibiotics to induce the virulence of these pathogens makes it increasingly difficult to rely on antibiotics to treat gastrointestinal infections. The probiotic E. coli strain Nissle 1917 (EcN) is the active component of the pharmaceutical preparation Mutaflor® and has been successfully used in the treatment of gastrointestinal disorders. Gut bacteriophages are dominant players in maintaining the microbial homeostasis in the gut, however, their interaction with incoming probiotic bacteria remains to be at conception. The presence of bacteriophages in the gut makes it inevitable for any probiotic bacteria to be phage resistant, in order to survive and successfully colonize the gut. This study addresses the phage resistance of EcN, specifically against lytic T4 phage infection. From various experiments we could show that i) EcN is resistant towards T4 phage infection, ii) EcN’s K5 polysaccharide capsule plays a crucial role in T4 phage resistance and iii) EcN’s lipopolysaccharide (LPS) inactivates T4 phages and notably, treatment with the antibiotic polymyxin B which neutralizes the LPS destroyed the phage inactivation ability of isolated LPS from EcN. Our results further indicate that N-acetylglucosamine at the distal end of O6 antigen in EcN’s LPS could be the interacting partner with T4 phages. From our findings, we have reported for the first time, the role of EcN’s K5 capsule and LPS in its defense against T4 phages. In addition, by inactivating the T4 phages, EcN also protects E. coli K-12 strains from phage infection in tri-culture experiments. The combination of the identified properties is not found in other tested commensal E. coli strains. Furthermore, our research highlights phage resistance as an additional safety feature of EcN, a clinically successful probiotic E. coli strain.
2019-08-27 | GSE135946 | GEO
Project description:Trichuris muris, the mouse whipworm is used as a laboratory model of the human parasite T. trichuira - a gastrointestinal nematode. Three laboratory isolates of T. muris exist: the E, J and S isolates. Previous data has shown that the S isolate survives to chronicity in C57BL/6 mice unlike the E and J isolates which are expelled. The ability of the S isolate to persist is still unclear. Microarray analysis of gut samples from mice infected with either the E or S isolates of T. muris for 7 days was used to determine early changes in gene expression that may later determine the outcome of infection.
2010-02-26 | E-MEXP-1795 | biostudies-arrayexpress
Project description:Purpose: Discovery of curative therapies for renal cell carcinoma (RCC) is hampered by lack of authentic preclinical models. Tumorgrafts, generated by direct implantation of patient-derived tissues into mice, have demonstrated superior ability to predict therapeutic response. We evaluated âtissue slice graftsâ (TSGs) as an improved tumorgraft model of RCC. Experimental Design: Cores of fresh RCC were precision-cut at 300-μm and implanted under the renal capsule of RAG2-/-γC-/- mice. Engraftment rate, histology, biomarker expression, genetic fidelity and metastatic potential were evaluated. Magnetic resonance imaging (MRI) was tested as a non-invasive method to measure tumor volume, and response to a targeted therapy was determined. Results: All 13 cases of RCC engrafted and displayed characteristic histology and biomarkers. TSG volume quantified non-invasively by MRI highly correlated with graft weights, providing a unique tool for monitoring orthotopic growth. Moreover, in 2 cases, cancer cells from TSGs metastasized to clinically relevant sites, including bone. Microarray analysis and DNA sequencing demonstrated a high degree of correlation of global gene expression and VHL status between TSGs and parental tumors. Treatment of TSGs with sunitinib significantly decreased graft weight and mean vessel density compared to controls. Conclusions: The TSG model of RCC faithfully recapitulates tumor pathology, gene expression, genetic mutation and drug response. The high engraftment rate and metastatic potential of this authentic model, in conjunction with the ability to generate large first-generation animal cohorts and to quantitate tumor volume at the orthotopic site by MRI, proffer significant advantages compared to other preclinical platforms. Three pairs of tissue slice graftes and parent tumors were included in the study. Tissue slice grafts and parent tumors were preserved in Allprotect tissue reagent (Qiagen, Valencia, CA) at -20°C prior to RNA extraction using an AllPrep DNA/RNA/Protein Mini Kit (Qiagen, Valencia, CA). The quality of RNA was determined using an Agilent 2100 Bioanalyzer (Agilent Biotechnologies, Santa Clara, CA). Microarray hybridization was performed using Illumina Human HT-12 v4 Beadchips (Illumina Inc., San Diego, CA) according to the manufacturerâs directions. Expression data was rank invariant normalized using BeadStudio software (Illumina Inc.).
2016-07-03 | E-GEOD-44548 | biostudies-arrayexpress