carnitine has been researched along with Colitis, Granulomatous in 10 studies
| Excerpt | Relevance | Reference |
|---|---|---|
| "Carnitine transport was very rapid and Na+ dependent (10s)." | 1.38 | Expression and functional analysis of intestinal organic cation/L-carnitine transporter (OCTN) in Crohn's disease. ( Bitton, A; Charlebois, P; Dionne, S; Elimrani, I; Girardin, M; Goyette, P; Levy, E; Qureshi, I; Rioux, J; Seidman, EG, 2012) |
| "The carnitine ester profile was determined using ESI triple quadrupole tandem MS." | 1.34 | Plasma carnitine ester profiles in Crohn's disease patients characterized for SLC22A4 C1672T and SLC22A5 G-207C genotypes. ( Bene, J; Figler, M; Gasztonyi, B; Horváth, K; Komlósi, K; Magyari, L; Melegh, B; Miheller, P; Mózsik, G; Talián, G; Tulassay, Z, 2007) |
| "Crohn disease is a chronic, inflammatory disease of the gastrointestinal tract." | 1.32 | Functional variants of OCTN cation transporter genes are associated with Crohn disease. ( Amos, CI; Cescon, D; Greenberg, G; Griffiths, AM; Gu, X; Huang, Q; Newman, B; Peltekova, VD; Rubin, LA; Siminovitch, KA; St George-Hyslop, PH; Van Oene, M; Wintle, RF, 2004) |
| "In patients with bacterial infections the granulocyte carnitine concentrations (126." | 1.29 | The variation of carnitine content in human blood cells during disease--a study in bacterial infection and inflammatory bowel disease. ( Böhles, H; Demirkol, M; Sewell, AC, 1994) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 1 (10.00) | 18.7374 |
| 1990's | 1 (10.00) | 18.2507 |
| 2000's | 5 (50.00) | 29.6817 |
| 2010's | 2 (20.00) | 24.3611 |
| 2020's | 1 (10.00) | 2.80 |
| Authors | Studies |
|---|---|
| Lamhonwah, AM | 1 |
| Skaug, J | 1 |
| Scherer, SW | 1 |
| Tein, I | 1 |
| Li, P | 1 |
| Wang, Y | 1 |
| Luo, J | 1 |
| Zeng, Q | 1 |
| Wang, M | 1 |
| Bai, M | 1 |
| Zhou, H | 1 |
| Wang, J | 1 |
| Jiang, H | 1 |
| Talián, G | 2 |
| Lakner, L | 1 |
| Bene, J | 2 |
| Komlósi, K | 2 |
| Horváth, K | 2 |
| Gasztonyi, B | 2 |
| Miheller, P | 2 |
| Figler, M | 2 |
| Mózsik, G | 2 |
| Tulassay, Z | 2 |
| Melegh, B | 2 |
| Pochini, L | 1 |
| Scalise, M | 1 |
| Galluccio, M | 1 |
| Pani, G | 1 |
| Siminovitch, KA | 2 |
| Indiveri, C | 1 |
| Girardin, M | 1 |
| Dionne, S | 1 |
| Goyette, P | 1 |
| Rioux, J | 1 |
| Bitton, A | 1 |
| Elimrani, I | 1 |
| Charlebois, P | 1 |
| Qureshi, I | 1 |
| Levy, E | 1 |
| Seidman, EG | 1 |
| Peltekova, VD | 1 |
| Wintle, RF | 1 |
| Rubin, LA | 1 |
| Amos, CI | 1 |
| Huang, Q | 1 |
| Gu, X | 1 |
| Newman, B | 1 |
| Van Oene, M | 1 |
| Cescon, D | 1 |
| Greenberg, G | 1 |
| Griffiths, AM | 1 |
| St George-Hyslop, PH | 1 |
| Magyari, L | 1 |
| Shekhawat, PS | 1 |
| Srinivas, SR | 1 |
| Matern, D | 1 |
| Bennett, MJ | 1 |
| Boriack, R | 1 |
| George, V | 1 |
| Xu, H | 1 |
| Prasad, PD | 1 |
| Roon, P | 1 |
| Ganapathy, V | 1 |
| Demirkol, M | 1 |
| Sewell, AC | 1 |
| Böhles, H | 1 |
| Böhmer, T | 1 |
| Rydning, A | 1 |
| Solberg, HE | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| In Vivo Study of Safety, Tolerability and Dosing Effect on SMN mRNA and Protein Levels of Valproic Acid in Patients With Spinal Muscular Atrophy[NCT00374075] | Phase 1 | 42 participants | Interventional | 2003-09-30 | Completed | ||
| Phase I/II Trial of Valproic Acid and Carnitine in Infants With Spinal Muscular Atrophy Type I (CARNI-VAL Type I)[NCT00661453] | Phase 1/Phase 2 | 40 participants (Actual) | Interventional | 2008-04-30 | Completed | ||
| Multi-center Phase II Trial of Valproic Acid and Carnitine in Patients With Spinal Muscular Atrophy (SMA CARNI-VAL Trial)[NCT00227266] | Phase 2 | 94 participants (Actual) | Interventional | 2005-09-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
(NCT00661453)
Timeframe: -2 weeks, time 0, 3 months, 6 months
| Intervention | g (Mean) | |||||
|---|---|---|---|---|---|---|
| Lean Mass Baseline | Lean Mass 3 months | Lean Mass 6 months | Fat Mass Baseline | Fat Mass 3 months | Fat Mass 6 months | |
| SMA Type 1 | 4317.15 | 4993.92 | 5133.83 | 3011.37 | 3618.25 | 4316.08 |
The maximum Compound Motor Action Potential (CMAP) is a measurement obtained through EMG testing that is associated with disease progression. In this study, we measure the maximum CMAP by stimulating one nerve in the hand and measuring the response of the muscle. This is done multiple times, the outcome used is the highest peak, or response observed. (NCT00227266)
Timeframe: 1 month prior to official enrollment, beginning of study (0 months), 6 months, 12 months (data point not available)
| Intervention | mV (Mean) | |
|---|---|---|
| Baseline | 6 months | |
| Cohort 1a Sitters Placebo Then Treatment | 2.28 | 2.32 |
| Cohort 1b Sitters Treatment | 2.93 | 2.37 |
| Cohort 2 Standers and Walkers - Treatment | 5.52 | 6.56 |
The maximum Compound Motor Action Potential (CMAP) is a measurement obtained through EMG testing that is associated with disease progression. In this study, we measure the maximum CMAP by stimulating one nerve in the hand and measuring the response of the muscle. This is done multiple times, the outcome used is the highest peak, or response observed. (NCT00227266)
Timeframe: 1 month prior to official enrollment, beginning of study (0 months), 6 months, 12 months (data point not available)
| Intervention | mV (Median) | |
|---|---|---|
| Baseline | 6 months | |
| Cohort 1a Sitters Placebo Then Treatment | 1.91 | 1.44 |
| Cohort 1b Sitters Treatment | 2.2 | 1.8 |
| Cohort 2 Standers and Walkers - Treatment | 5.3 | 5.85 |
The maximum Compound Motor Action Potential (CMAP) area is a measurement obtained through EMG testing that is associated with disease progression. In this study, we measure the maximum CMAP by stimulating one nerve in the hand and measuring the response of the muscle. This procedure is repeated multiple times. The maximum area is the response that results in the largest area under the response curve. (NCT00227266)
Timeframe: 1 month prior to official enrollment, beginning of study (0 months), 6 months, 12 months (data point not available)
| Intervention | mVms (Mean) | |
|---|---|---|
| Baseline | 6 months | |
| Cohort 1a Sitters Placebo Then Treatment | 5.46 | 5.28 |
| Cohort 1b Sitters Treatment | 5.45 | 5.26 |
| Cohort 2 Standers and Walkers - Treatment | 14.85 | 16.26 |
The maximum Compound Motor Action Potential (CMAP) area is a measurement obtained through EMG testing that is associated with disease progression. In this study, we measure the maximum CMAP by stimulating one nerve in the hand and measuring the response of the muscle. This procedure is repeated multiple times. The maximum area is the response that results in the largest area under the response curve. (NCT00227266)
Timeframe: 1 month prior to official enrollment, beginning of study (0 months), 6 months, 12 months (data point not available)
| Intervention | mVms (Median) | |
|---|---|---|
| Baseline | 6 months | |
| Cohort 1a Sitters Placebo Then Treatment | 3.6 | 3.74 |
| Cohort 1b Sitters Treatment | 4.6 | 3.4 |
| Cohort 2 Standers and Walkers - Treatment | 13.65 | 16.85 |
Comparison of Modified Hammersmith Change from baseline to 6 months. Scores range from 0 to 40. A higher score indicates a better outcome. This scale is used to assess gross motor abilities of non-ambulant children with SMA in multiple research trials as well as in clinical settings. (NCT00227266)
Timeframe: 0 months, 6 months
| Intervention | Score (Mean) | ||
|---|---|---|---|
| Baseline visit (0 weeks) | 6 Month visit (V2) | Change from Baseline | |
| Cohort 1a Sitters Placebo Then Treatment | 20.0 | 20.6 | 0.6 |
| Cohort 1b Sitters Treatment | 16.6 | 16.8 | 0.2 |
"Baseline Modified Hammersmith Extend testing. The baseline test is the score they receive during their screening visits. This scale ranges from 0 to 56. A higher score indicates a better outcome.~This scale is used to assess gross motor abilities of children with SMA in multiple research trials as well as in clinical settings." (NCT00227266)
Timeframe: 1 month prior to enrollment, at enrollment (0 months)
| Intervention | Score (Mean) | |
|---|---|---|
| Modified Hammersmith Extend at S1 (-4 weeks) | Modified Hammersmith Extend at S2 (0 weeks) | |
| Cohort 2 Experimental | 47.0 | 48.3 |
10 other studies available for carnitine and Colitis, Granulomatous
| Article | Year |
|---|---|
A third human carnitine/organic cation transporter (OCTN3) as a candidate for the 5q31 Crohn's disease locus (IBD5).
Topics: Animals; Biological Transport; Carnitine; Cells, Cultured; Chromosomes, Human, Pair 5; Crohn Disease | 2003 |
Downregulation of OCTN2 by cytokines plays an important role in the progression of inflammatory bowel disease.
Topics: Adult; Animals; Anti-Inflammatory Agents; Carnitine; Cell Line; Colitis, Ulcerative; Crohn Disease; | 2020 |
Plasma carnitine ester profiles in Crohn's disease and ulcerative colitis patients with different IGR2230a_1 genotypes.
Topics: Adult; Carnitine; Case-Control Studies; Colitis, Ulcerative; Crohn Disease; Esters; Female; Genotype | 2009 |
The human OCTN1 (SLC22A4) reconstituted in liposomes catalyzes acetylcholine transport which is defective in the mutant L503F associated to the Crohn's disease.
Topics: Acetylcarnitine; Acetylcholine; Adenosine Triphosphate; Amino Acid Substitution; Betaine; Biological | 2012 |
Expression and functional analysis of intestinal organic cation/L-carnitine transporter (OCTN) in Crohn's disease.
Topics: Adolescent; Adult; Aged; Analysis of Variance; Biological Transport; Carnitine; Child; Colitis, Ulce | 2012 |
Functional variants of OCTN cation transporter genes are associated with Crohn disease.
Topics: Amino Acid Sequence; Amino Acid Substitution; Carnitine; Carrier Proteins; Chromosomes, Human, Pair | 2004 |
Plasma carnitine ester profiles in Crohn's disease patients characterized for SLC22A4 C1672T and SLC22A5 G-207C genotypes.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Carnitine; Crohn Disease; Esters; Female; Gene Frequency | 2007 |
Spontaneous development of intestinal and colonic atrophy and inflammation in the carnitine-deficient jvs (OCTN2(-/-)) mice.
Topics: Amino Acid Transport Systems; Animals; Atrophy; Carnitine; Colon; Crohn Disease; Disease Models, Ani | 2007 |
The variation of carnitine content in human blood cells during disease--a study in bacterial infection and inflammatory bowel disease.
Topics: Acute Disease; Adolescent; Adult; Bacterial Infections; Carnitine; Child; Chronic Disease; Crohn Dis | 1994 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |
Carnitine levels in human serum in health and disease.
Topics: Acetyl Coenzyme A; Acetyltransferases; Anorexia Nervosa; Benzoates; Carbon Radioisotopes; Cardiomega | 1974 |