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> Disorders > Disease or Syndrome > Ulcerative Colitis

Ulcerative Colitis

Ulcerative Colitis is a chronic inflammatory bowel disease characterized by continuous inflammation and ulceration of the colonic mucosa, typically beginning in the rectum and extending proximally.
Symptoms may include bloody diarrhoea, abdominal pain, and weight loss.
The cause is unknown but is thought to involve an abnormal immune response.
Effective management often requires a combination of medication, dietary changes, and occasionally surgery.
Early diagnosis and appropriate treatment are crucial to minimize complications and improve quality of life for patients.

Most cited protocols related to «Ulcerative Colitis»

1
Rosiglitazone for Ulcerative Colitis: A Placebo-Controlled Trial
Data for this study were acquired from a recently completed placebo-controlled randomized trial of rosiglitazone for mild to moderately active ulcerative colitis (clinicaltrials.gov #NCT00065065) which has been described in greater detail previously.7 (link) The trial used a slight modification of the Mayo score to assess disease activity (Table 1). Specifically, the bleeding component as described in the Mayo index was modified such that a score of 3 required both visible blood in 50% or more of bowel movements and at least some bowel movements with blood alone.
The study included 105 patients with mild to moderately active disease defined as a total DAI score of 4 to 10, inclusively. Patients were randomized in a 1:1 ratio to receive either rosiglitazone 4 mg or placebo twice daily for 12 weeks. Disease activity was measured at randomization and every four weeks thereafter until week 12, however lower endoscopy was only completed at week 0 and week 12, such that only a partial Mayo score (9 point scale that excludes the endoscopic appearance of the mucosa) could be calculated at the interim visits. In the very early accrual period of the study, a follow-up visit was included at week 2. Without knowledge of the response rates in either arm, the Data and Safety Monitoring Board (DSMB) requested that the week 2 follow-up evaluation be eliminated with the hopes of minimizing the placebo response rate and maximizing recruitment and retention.6 (link), 8 (link), 9 (link) Eighteen patients completed the week 2 follow-up visit.
During the course of the study, patients could be treated with other conventional medications used to treat active ulcerative colitis including mesalamine, oral corticosteroids, immunomodulators, or topical therapies (mesalamine or corticosteroids) at stable doses. Use of corticosteroids at doses greater than 20mg per day of prednisone or the equivalent was an exclusion criterion. Steroid tapering was not permitted during the study.
In anticipation of this sub-study, at each visit we also included questions about change in disease activity compared to the previous visit and compared to the randomization visit on a global seven-point scale (Table 2). The choices included much better, moderately better, a little better, unchanged, a little worse, moderately worse, and much worse. Patients also graded their current disease activity at each visit on a 6 point Likert scale – perfect, very good (minimal symptoms), good (only mild symptoms), moderately active, moderately severe, or severe. Data on quality of life were measured with the Inflammatory Bowel Disease Questionnaire (IBDQ) authored by Dr. Jan Irvine under license from McMaster University, Hamilton, Canada.10 (link)
Lewis J.D., Chuai S., Nessel L., Lichtenstein G.R., Aberra F.N, & Ellenberg J.H. (2008). Use of the Non-invasive Components of the Mayo Score to Assess Clinical Response in Ulcerative Colitis. Inflammatory bowel diseases, 14(12), 1660-1666.
Publication 2008
Adrenal Cortex Hormones BLOOD Clinical Trials Data Monitoring Committees Defecation Endoscopy Endoscopy, Gastrointestinal Immunologic Adjuvants Inflammatory Bowel Diseases Mesalamine Mucous Membrane Patients Pharmaceutical Preparations Placebos Prednisone Retention (Psychology) Rosiglitazone Steroids Ulcerative Colitis
2
Comprehensive IBD Association Analysis
Prior to association testing, we removed all samples that were included in previous IBD GWAS meta-analyses (Supplementary Table 1). We then tested for association to ulcerative colitis, Crohn’s disease and IBD separately within the sequenced samples and new GWAS using SNPTEST v2.5, performing an additive frequentist association test conditioned on the first ten principal components for each cohort. We filtered out variants with minor allele frequency (MAF) < 0.1%, INFO < 0.4, or strong evidence for deviations from HWE in controls (pHWE<1x10-7).
de Lange K.M., Moutsianas L., Lee J.C., Lamb C.A., Luo Y., Kennedy N.A., Jostins L., Rice D.L., Gutierrez-Achury J., Ji S.G., Heap G., Nimmo E.R., Edwards C., Henderson P., Mowat C., Sanderson J., Satsangi J., Simmons A., Wilson D.C., Tremelling M., Hart A., Mathew C.G., Newman W.G., Parkes M., Lees C.W., Uhlig H., Hawkey C., Prescott N.J., Ahmad T., Mansfield J.C., Anderson C.A, & Barrett J.C. (2017). Genome-wide association study implicates immune activation of multiple integrin genes in inflammatory bowel disease. Nature genetics, 49(2), 256-261.
Publication 2016
Crohn Disease Genome-Wide Association Study Ulcerative Colitis
3
Crohn's and Ulcerative Colitis GWAS Meta-Analysis
The GWAS cohorts and QC are described in detail in Jostins & Ripke et al. (2012). Briefly, seven Crohn’s disease and eight ulcerative colitis collections with genome-wide SNP data were combined. Samples were genotyped on a combination of Affymetrix GeneChip Human Mapping 500K, Affymetrix Genome-Wide Human SNP Array 6.0, Illumina HumanHap300 BeadChip and Illumina HumanHap550 BeadChip arrays. After SNP and sample QC, the Crohn's disease data consisted of 5,956 cases and 14,927 controls, the ulcerative colitis data consisted of 6,968 cases and 20,464 controls, and Crohn's disease+ulcerative colitis combined (IBD) data consisted of 12,882 cases and 21,770 controls. The number of SNPs per collection varied between 290,000 and 780,000.
Liu J.Z., van Sommeren S., Huang H., Ng S.C., Alberts R., Takahashi A., Ripke S., Lee J.C., Jostins L., Shah T., Abedian S., Cheon J.H., Cho J., Dayani N.E., Franke L., Fuyuno Y., Hart A., Juyal R.C., Juyal G., Kim W.H., Morris A.P., Poustchi H., Newman W.G., Midha V., Orchard T.R., Vahedi H., Sood A., Sung J.Y., Malekzadeh R., Westra H.J., Yamazaki K., Yang S.K., Barrett J.C., Alizadeh B.Z., Parkes M., BK T., Daly M.J., Kubo M., Anderson C.A, & Weersma R.K. (2015). Association analyses identify 38 susceptibility loci for inflammatory bowel disease and highlight shared genetic risk across populations. Nature genetics, 47(9), 979-986.
Publication 2015
Crohn Disease Gene Chips Genome Genome, Human Genome-Wide Association Study Homo sapiens Single Nucleotide Polymorphism Ulcerative Colitis
4
Comprehensive IBD Association Analysis
Prior to association testing, we removed all samples that were included in previous IBD GWAS meta-analyses (Supplementary Table 1). We then tested for association to ulcerative colitis, Crohn’s disease and IBD separately within the sequenced samples and new GWAS using SNPTEST v2.5, performing an additive frequentist association test conditioned on the first ten principal components for each cohort. We filtered out variants with minor allele frequency (MAF) < 0.1%, INFO < 0.4, or strong evidence for deviations from HWE in controls (pHWE<1x10-7).
de Lange K.M., Moutsianas L., Lee J.C., Lamb C.A., Luo Y., Kennedy N.A., Jostins L., Rice D.L., Gutierrez-Achury J., Ji S.G., Heap G., Nimmo E.R., Edwards C., Henderson P., Mowat C., Sanderson J., Satsangi J., Simmons A., Wilson D.C., Tremelling M., Hart A., Mathew C.G., Newman W.G., Parkes M., Lees C.W., Uhlig H., Hawkey C., Prescott N.J., Ahmad T., Mansfield J.C., Anderson C.A, & Barrett J.C. (2017). Genome-wide association study implicates immune activation of multiple integrin genes in inflammatory bowel disease. Nature genetics, 49(2), 256-261.
Publication 2016
Crohn Disease Genome-Wide Association Study Ulcerative Colitis
5
Expanding PheWAS Phenotype Categorization
In this study, we revised and expanded our earlier PheWAS phenotype categorization to a total of 1,645 phenotypes identified from International Classification of Disease, Ninth revision, Clinical Modification (ICD9) codes. (Our initial PheWAS phenotype categorization included 744 phenotypes9 (link).) The ICD9 coding system is divided into four components: diseases, signs and symptoms (“three digit” codes, 001–999), external causes of injury (“E” codes), procedures (“two digit” codes 00.0–99.9) and supplemental classifications (“V” codes). The prior PheWAS code groupings included only diseases, signs and symptoms (three digit) ICD9 codes9 (link). We revised and expanded the PheWAS phenotypes by (i) adding V codes (commonly used to record personal histories of given diseases) and E codes (which refer to external causes of injury) to the PheWAS code mapping, (ii) redesigning the code system to be hierarchical, such that one phenotype could be a parent of another subphenotype (e.g., cardiac arrhythmias is a parent of atrial fibrillation, atrial flutter and other arrhythmias), and (iii) including more granular phenotypes into the coding system (e.g., “type 1 diabetes with ketoacidosis”). Creation of hierarchical phenotypes included creation of phenotypes not present in the ICD9 billing hierarchy, such as “inflammatory bowel disease” as the parent phenotype for “Crohn’s disease” and “ulcerative colitis.” In this process, we were guided by the hierarchical organization of the Clinical Classifications Software (CCS) produced by the Agency for Healthcare Research and Quality42 (link); the 2011 version of the CCS contains 727 phenotypes. The resulting PheWAS code group currently contains 1,645 phenotypes, 1,358 of which had at least 25 cases (a prevalence of 0.18% in our data set) in the eMERGE cohort, our threshold for these analyses. The current version of the PheWAS codes, with ICD9 mappings and control groups, is available from http://knowledgemap.mc.vanderbilt.edu/research/content/phewas.
Denny J.C., Bastarache L., Ritchie M.D., Carroll R.J., Zink R., Mosley J.D., Field J.R., Pulley J.M., Ramirez A.H., Bowton E., Basford M.A., Carrell D.S., Peissig P.L., Kho A.N., Pacheco J.A., Rasmussen L.V., Crosslin D.R., Crane P.K., Pathak J., Bielinski S.J., Pendergrass S.A., Xu H., Hindorff L.A., Li R., Manolio T.A., Chute C.G., Chisholm R.L., Larson E.B., Jarvik G.P., Brilliant M.H., McCarty C.A., Kullo I.J., Haines J.L., Crawford D.C., Masys D.R, & Roden D.M. (2013). Systematic comparison of phenome-wide association study of electronic medical record data and genome-wide association study data. Nature biotechnology, 31(12), 1102-1110.
Publication 2013
Atrial Fibrillation Atrial Flutter Cardiac Arrhythmia Crohn Disease Diabetic Ketoacidosis Fingers Inflammatory Bowel Diseases Injuries Parent Phenotype Ulcerative Colitis

Most recents protocols related to «Ulcerative Colitis»

1
Ingestible Device for Ulcerative Colitis Treatment
Not available on PMC !

Example 12

As a proof of concept, the patient population of this study is patients that (1) have moderate to severe ulcerative colitis, regardless of extent, and (2) have had an insufficient response to a previous treatment, e.g., a conventional therapy (e.g., 5-ASA, corticosteroid, and/or immunosuppressant) or a FDA-approved treatment. In this placebo-controlled eight-week study, patients are randomized. All patient undergo a colonoscopy at the start of the study (baseline) and at week 8. Patients enrolled in the study are assessed for clinical status of disease by stool frequency, rectal bleeding, abdominal pain, physician's global assessment, and biomarker levels such as fecal calprotectin and hsCRP. The primary endpoint is a shift in endoscopy scores from Baseline to Week 8. Secondary and exploratory endpoints include safety and tolerability, change in rectal bleeding score, change in abdominal pain score, change in stool frequency, change in partial Mayo score, change in Mayo score, proportion of subjects achieving endoscopy remission, proportion of subjects achieving clinical remission, change in histology score, change in biomarkers of disease such as fecal calprotectin and hsCRP, level of adalimumab in the blood/tissue/stool, change in cytokine levels (e.g., TNFα, IL-6) in the blood and tissue.

FIG. 72 describes an exemplary process of what would occur in clinical practice, and when, where, and how the ingestible device will be used. Briefly, a patient displays symptoms of ulcerative colitis, including but not limited to: diarrhea, bloody stool, abdominal pain, high c-reactive protein (CRP), and/or high fecal calprotectin. A patient may or may not have undergone a colonoscopy with diagnosis of ulcerative colitis at this time. The patient's primary care physician refers the patient. The patient undergoes a colonoscopy with a biopsy, CT scan, and/or MRI. Based on this testing, the patient is diagnosed with ulcerative colitis. Most patients are diagnosed with ulcerative colitis by colonoscopy with biopsy. The severity based on clinical symptoms and endoscopic appearance, and the extent, based on the area of involvement on colonoscopy with or without CT/MRI is documented. Treatment is determined based on diagnosis, severity and extent.

For example, treatment for a patient that is diagnosed with ulcerative colitis is an ingestible device programmed to release a single bolus of a therapeutic agent, e.g., 40 mg adalimumab, in the cecum or proximal to the cecum. Prior to administration of the treatment, the patient is fasted overnight and is allowed to drink clear fluids. Four hours after swallowing the ingestible device, the patient can resume a normal diet. An ingestible device is swallowed at the same time each day. The ingestible device is not recovered.

In some embodiments, there may be two different ingestible devices: one including an induction dose (first 8 to 12 weeks) and a different ingestible device including a different dose or a different dosing interval.

In some examples, the ingestible device can include a mapping tool, which can be used after 8 to 12 weeks of induction therapy, to assess the response status (e.g., based on one or more of the following: drug level, drug antibody level, biomarker level, and mucosal healing status). Depending on the response status determined by the mapping tool, a subject may continue to receive an induction regimen or maintenance regimen of adalimumab.

In different clinical studies, the patients may be diagnosed with Crohn's disease and the ingestible devices (including adalimumab) can be programmed to release adalimumab in the cecum, or in both the cecum and transverse colon.

In different clinical studies, the patients may be diagnosed with illeocolonic Crohn's disease and the ingestible devices (including adalimumab) can be programmed to release adalimumab in the late jejunum or in the jejunum and transverse colon.

US11857669B2. Treatment of a disease of the gastrointestinal tract with a JAK inhibitor and devices (2024-01-02). BIORA THERAPEUTICS, INC. [US]. Inventors: Mitchell Lawrence Jones [US], Sharat Singh [US], Christopher Loren Wahl [US], Harry Stylli [US].
Patent 2024
Abdominal Pain Adalimumab Adrenal Cortex Hormones Biological Markers Biopsy BLOOD Cecum Colonoscopy C Reactive Protein Crohn Disease Cytokine Diarrhea Diet Endoscopy Endoscopy, Gastrointestinal Feces Homo sapiens Immunoglobulins Immunosuppressive Agents Jejunum Leukocyte L1 Antigen Complex Medical Devices Mesalamine Mucous Membrane Neoadjuvant Therapy Patient Care Management Patients Pharmaceutical Preparations Placebos Primary Care Physicians Safety Therapeutics Tissues Transverse Colon Treatment Protocols Tumor Necrosis Factor-alpha Ulcerative Colitis X-Ray Computed Tomography
2
Quantifying CD30L Expression on Activated Primary Lymphocytes
Not available on PMC !

Example 4

Peripheral blood mononuclear cells (PBMCs) were isolated from freshly collected whole blood from Ulcerative Colitis (UC) and Crohn's Disease (CD) patients, by conventional density gradient centrifugation. To induce CD30L expression on primary lymphocytes, the isolated cells were stimulated overnight with Phorbol 12-myristate 13-acetate (PMA) and ionomycin. The next day, the stimulated cells, along with non-stimulated cells kept as control, were collected, washed and incubated on ice with increasing concentrations of fluorescently labeled anti-CD30L antibodies or isotype control (from 0.001 nM to 60 nM). After washing to remove unbound antibodies, the cells were fixed in a paraformaldehyde solution and analyzed by flow cytometry to quantify cell surface antibody binding. Typical results from this assay are shown in Table 7.

TABLE 7
Binding to primary lymphocytes from UC and
CD patients stimulated with PMA/ionomycin.
Patient 1Patient 2Patient 3Patient 4
(CD, #04-021)(UC, #03-041)(UC, #02-180)(CD, #01-051)
AntibodyBindingBindingBindingBinding
CloneEC50 (nM)EC50 (nM)EC50 (nM)EC50 (nM)
Ref1 (HC of3.633.123.072.82
SEQ ID NO:
768 & LC of
SEQ ID NO:
769)
17.455.435.574.53
22.401.551.711.72

US11866505B2. Anti-CD30L antibodies and uses thereof (2024-01-09). PROMETHEUS BIOSCIENCES, INC. [US], DR. FALK PHARMA GMBH [DE]. Inventors: Jessie-Farah Fecteau [US], Mark Renshaw [US], Johan Fransson [US], Olivier Laurent [US], Burton Barnett [US].
Patent 2024
Anti-Antibodies Antibodies APEX1 protein, human Biological Assay BLOOD Cells Centrifugation, Density Gradient Clone Cells Crohn Disease Flow Cytometry Immunoglobulin Isotypes Immunoglobulins Ionomycin Lymphocyte paraform Patients PBMC Peripheral Blood Mononuclear Cells Tetradecanoylphorbol Acetate Ulcerative Colitis
3
Evaluating DSS-Induced Colitis in Mice
Not available on PMC !

Example 20

Colitis in mouse was induced by adding 3% DSS (dextran sulfate sodium) in the drinking water for 12 consecutive days. Besides DSS placement, mice were daily treated with GLP-2 analogs (40 μg/kg/day) [GLP-2G is the GLP2 sequence with G2S mutation and is a known drug called teduglutide]. Cyclosporine A (20 mg/kg/day) was used for the positive control group and PBS for the negative control group. During the experiment period, body weight was measured every day.

Intestinal Weight Body Weight Measurement

Animals were sacrificed after 12 days of treatment. Small intestine was immediately excited and flushed with PBS. After PBS was gently squished out, intestinal weight was weighed using an analytical balance. Intestinal vs. body weight ratio was then calculated and analyzed.

Body weight and intestine weight versus body weight in DSS-induced colitis mice after daily administration of mTA68 for 12 days are shown in FIG. 23.

US11865160B2. Modified therapeutic agents, stapled peptide lipid conjugates, and compositions thereof (2024-01-09). THE SCRIPPS RESEARCH INSTITUTE [US]. Inventors: Weijun Shen [US], Pengyu Yang [US], Huafei Zou [US], Peter G. Schultz [US].
Patent 2024
Aftercare Animals Body Weight Colitis Cyclosporine Dextran Sulfate Sodium Intestines Intestines, Small Mus Mutation Pharmaceutical Preparations teduglutide Ulcerative Colitis
4
Synthesis of 5-amino-2-(1-(3-methoxypropyl)-2,6-dioxopiperidin-3-yl)isoindolin-1,3-dione
Not available on PMC !

Example 18

Preparation of 5-amino-2-(1-(3-methoxypropyl)-2,6-dioxopiperidin-3-yl)isoindolin-1,3-dione

Using the preparation process in Example 4, 5-nitrophthalic anhydride and 1-(3-methoxypropyl)-3-amino-2,6-piperidinedione acetate were reacted to prepare 5-nitro-2-(1-(3-methoxypropyl)-2,6-dioxopiperidin-3-yl)-isoindolin-1,3-dione as a yellowish oily product (1.118 g) (HPLC purity: 98.44%). Yield: 20%. MS(m/e): 376.25 (M+H+).

Using the preparation process in Example 7, 5-nitro-2-(1-(3-methoxypropyl)-2,6-dioxopiperidin-3-yl)-isoindolin-1,3-dione was used to give the title compound as a yellowish solid (0.697 g) (HPLC purity: 97.79%). Yield: 67.7%.

1HNMR(CDCl3, 400 MHz) δ 7.624-7.603 (d, 1H), 7.031-7.027 (d, 1H), 6.861-6.835 (dd, 1H), 4.925-4.879 (m, 1H), 3.977-3.863 (m, 2H), 3.421-3.390 (t, 2H), 3.301 (s, 3H), 2.969-2.922 (m, 1H), 2.820-2.676 (m, 2H), 2.108-2.056 (m, 1H), 1.869-1.794 (m, 2H). MS(m/e): 346.24 (M+H+).

US11873287B2. Piperidine-2,6-dione derivatives and ulcerative colitis treating (2024-01-16). TIANJIN HEMAY PHARMACEUTICAL SCI-TECH CO., LTD [CN], GANZHOU HEMAY PHARMACEUTICAL, CO., LTD [CN]. Inventors: Hesheng Zhang [CN], Guanghuai Zeng [CN].
Patent 2024
Acetate Anhydrides derivatives High-Performance Liquid Chromatographies Oils piperidine Ulcerative Colitis
5
FMT for Refractory IBD Patients
Adult IBD patients with active disease or IBD in remission with a confirmed diagnosis of Crohn’s disease (CD), ulcerative colitis (UC), or IBD-unclassified treated with FMT for rCDI were included. There were no specific exclusion criteria. All eligible patients provided informed consent at the participating centres at the moment of FMT according to local requirements.
van Lingen E.(., Baunwall S.(., Lieberknecht S.(., Benech N.(., Ianiro G.(., Sokol H.(., Gasbarrini A.(., Cammarota G.(., Eriksen M.(., van der Meulen-de Jong A.(., Terveer E.(., Verspaget H.(., Vehreschild M.(., Hvas C.(, & Keller J.(. (2023). Short- and long-term follow-up after fecal microbiota transplantation as treatment for recurrent Clostridioides difficile infection in patients with inflammatory bowel disease. Therapeutic Advances in Gastroenterology, 16, 17562848231156285.
Publication 2023
Adult Crohn Disease Diagnosis Patients Ulcerative Colitis

Top products related to «Ulcerative Colitis»

1
Dextran sulfate sodium (dss) by MP Biomedicals
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The DSS is a laboratory instrument designed for the separation and analysis of molecules and particles in complex samples. It utilizes a specialized technique called differential sedimentation to achieve precise separation and characterization of the components within a sample. The core function of the DSS is to provide accurate and reliable data on the size, distribution, and concentration of the analytes present, without interpretation or extrapolation on its intended use.
2
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TRIzol is a monophasic solution of phenol and guanidine isothiocyanate that is used for the isolation of total RNA from various biological samples. It is a reagent designed to facilitate the disruption of cells and the subsequent isolation of RNA.
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Iselect hd by Illumina
The ISelect HD is a high-density genotyping array designed for accurate and cost-effective genome-wide association studies (GWAS) and other genomic research applications. The array features a comprehensive content covering a wide range of genetic markers across the human genome.
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Manifest file immuno beadchip 11419691 b bpm by Illumina
The Manifest file Immuno_BeadChip_11419691_B.bpm is a core component of the Illumina platform, providing a detailed specification of the content and layout of the Immuno_BeadChip array. This file defines the genomic positions, probe sequences, and other critical information required for the accurate analysis of data generated from the Immuno_BeadChip. It serves as a fundamental reference for researchers and analysts working with this particular microarray platform.
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6
Affymetrix 500k chip by Thermo Fisher Scientific
The Affymetrix 500K chip is a high-density genotyping array designed for genome-wide association studies. It contains probes for the detection of over 500,000 single nucleotide polymorphisms (SNPs) across the human genome. The chip allows for the simultaneous analysis of a large number of genetic markers to identify associations between genetic variants and complex traits or diseases.
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Genomestudio data analysis software by Illumina
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GenomeStudio Data Analysis Software is a comprehensive platform for analyzing and interpreting data generated from Illumina's sequencing and microarray technologies. It provides tools for visualizing, managing, and analyzing genomic data. The software's core function is to enable researchers and scientists to explore, interpret, and derive insights from their genomic data.
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Histoacryl tissue glue by B. Braun
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Histoacryl tissue glue is a medical adhesive product manufactured by B. Braun. It is designed for use in various surgical procedures to aid in the closure and sealing of tissue.
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Human core exome array v12 by Illumina
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More about "Ulcerative Colitis"

Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) that causes chronic inflammation and ulceration of the colon and rectum.
It is characterized by continuous inflammation and damage to the inner lining of the large intestine, often beginning in the rectum and spreading upwards.
Symptoms of ulcerative colitis can include bloody diarrhea, abdominal pain, weight loss, and fatigue.
The exact cause is unknown, but it is thought to involve an abnormal immune response that triggers the inflammation.
Effective management of ulcerative colitis often requires a combination of medication, dietary changes, and sometimes surgery.
Medications like aminosalicylates, corticosteroids, and immunosuppressants can help control inflammation and symptoms.
Dietary modifications, such as avoiding certain trigger foods, can also be helpful.
Early diagnosis and appropriate treatment are crucial to minimize complications and improve the quality of life for patients.
Diagnostic tools like the DSS (dextran sulfate sodium) model, TRIzol reagent, and ISelect HD BeadChip can be used to study the disease and develop new therapies.
Genetic factors also play a role in ulcerative colitis, and techniques like the Affymetrix 500K chip and GenomeStudio Data Analysis Software can be used to analyze genetic variations associated with the condition.
Additionally, Histoacryl tissue glue may be used in some surgical procedures for ulcerative colitis.
Staying informed and working closely with healthcare providers is important for managing ulcerative colitis and improving outcomes for patients.
By understanding the latest research and advancements in this field, individuals can make informed decisions about their care and take an active role in their treatment.