INT204139

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Context Info
Confidence 0.23
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 4
Disease Relevance 0.90
Pain Relevance 1.96

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cell proliferation (BCAR1) cytosol (BCAR1) signal transduction (BCAR1)
cell adhesion (BCAR1) plasma membrane (BCAR1) cell division (BCAR1)
BCAR1 (Homo sapiens)
Pain Link Frequency Relevance Heat
diclofenac 48 100.00 Very High Very High Very High
Paracetamol 28 100.00 Very High Very High Very High
cINOD 20 100.00 Very High Very High Very High
Analgesic 16 100.00 Very High Very High Very High
carbamazepine 32 98.82 Very High Very High Very High
fluoxetine 8 5.00 Very Low Very Low Very Low
Bioavailability 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 20 100.00 Very High Very High Very High
Ulcers 8 97.64 Very High Very High Very High
Diabetes Mellitus 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Fig. 1Removal, during MBR and CAS treatment, of the analgesics and anti-inflammatory drugs naproxen (a), ketoprofen (b), ibuprofen (c), mefenamic acid (d), diclofenac (e), indomethacin (f), acetaminophen (g), and propyphenazone (h)Fig. 2Removal during MBR and CAS treatment of the antibiotics ofloxacin (a), sulfamethoxazole (b), and erythromycin (c), the ?
Positive_regulation (during) of Gene_expression (treatment) of CAS associated with paracetamol, inflammation, analgesic, cinod and diclofenac
1) Confidence 0.23 Published 2006 Journal Anal Bioanal Chem Section Body Doc Link PMC1805043 Disease Relevance 0.17 Pain Relevance 0.37
Fig. 1Removal, during MBR and CAS treatment, of the analgesics and anti-inflammatory drugs naproxen (a), ketoprofen (b), ibuprofen (c), mefenamic acid (d), diclofenac (e), indomethacin (f), acetaminophen (g), and propyphenazone (h)Fig. 2Removal during MBR and CAS treatment of the antibiotics ofloxacin (a), sulfamethoxazole (b), and erythromycin (c), the ?
Positive_regulation (during) of Gene_expression (treatment) of CAS associated with paracetamol, inflammation, analgesic, cinod and diclofenac
2) Confidence 0.23 Published 2006 Journal Anal Bioanal Chem Section Body Doc Link PMC1805043 Disease Relevance 0.24 Pain Relevance 0.49
Fig. 1Removal, during MBR and CAS treatment, of the analgesics and anti-inflammatory drugs naproxen (a), ketoprofen (b), ibuprofen (c), mefenamic acid (d), diclofenac (e), indomethacin (f), acetaminophen (g), and propyphenazone (h)Fig. 2Removal during MBR and CAS treatment of the antibiotics ofloxacin (a), sulfamethoxazole (b), and erythromycin (c), the ?
Positive_regulation (during) of Gene_expression (treatment) of CAS associated with paracetamol, inflammation, analgesic, cinod and diclofenac
3) Confidence 0.23 Published 2006 Journal Anal Bioanal Chem Section Body Doc Link PMC1805043 Disease Relevance 0.24 Pain Relevance 0.49
-blockers atenolol (d) and metoprolol (e), the anti-ulcer agent ranitidine (f), the antiepileptic drug carbamazepine (g), and the psychiatric drug paroxetine (h)Fig. 3Removal during MBR and CAS treatment of the lipid regulator and cholesterol-lowering statin drugs gemfibrozil (a), bezafibrate (b), clofibric acid (c), and pravastatin (d), the diuretic hydrochlorothiazide (e), and the hypoglycaemic agent glibenclamide (f)
Positive_regulation (during) of Gene_expression (treatment) of CAS associated with ulcers and carbamazepine
4) Confidence 0.23 Published 2006 Journal Anal Bioanal Chem Section Body Doc Link PMC1805043 Disease Relevance 0.26 Pain Relevance 0.60

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