Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The main pathogens of gram-negative infections are Neisseria gonorrhoeae, Neisseria meningitidis and Moraxella catarrhalis infection. N. Gonorrhoeae infection is one of the STD, but the chemotherapy for this infection is very easy because this pathogen is very susceptible to new quinolones. Meningococcal infection is very rare in Japan. Since 1980, M. catarrhalis is one of the important pathogen of respiratory infections such as acute bronchitis, pneumonia, chronic bronchitis. This pathogen also causes acute sinusitis and otitis. Most pathogenic strains of M. catarrhalis are beta-lactamase producing.
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PMID:[Gram-negative coccus infection]. 812 87

The purpose of the study is to compare a generic and a specific quality of life (QoL) instrument in the assessment of QoL in chronic bronchitis. Data from 320 patients were collected at acute exacerbation of chronic bronchitis (AECB), and from 230 patients during a subsequent stable phase (non-AECB), utilising both the specific St George's respiratory questionnaire (SGRQ) and the generic Nottingham health profile (NHP). Patients (maximum n = 200) reported significantly poorer QoL at AECB than at non-AECB for all domains except the SGRQ symptom domain (SRM = 0.02). The SGRQ was more sensitive than the NHP to QoL differences between patients. The correlations between the scores across the two assessments were generally higher for the SGRQ, with the correlations between the NHP and SGRQ being lower at AECB, suggesting that the instruments are measuring different constructs at AECB, with the SGRQ being less responsive to QoL change. Indeed, the NHP was generally more responsive to QoL change in terms of 'risk' and clinical factors, with the SGRQ symptom domain appearing particularly non-responsive. In conclusion, this study suggests that the condition-specific SGRQ, and particularly its symptom domain, is less responsive than the generic NHP to QoL change accompanying AECB. This reflects the construct of the symptom domain which measures chronic bronchitis symptoms over the previous year.
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PMID:Validity of the St George's respiratory questionnaire at acute exacerbation of chronic bronchitis: comparison with the Nottingham health profile. 1263 59

A 52-year-old man with well-controlled HIV infection taking ritonavir and increasing doses of inhaled fluticasone for chronic bronchitis developed thrush. Within days of discontinuing fluticasone and initiating fluconazole, he presented with fatigue, malaise, lower-extremity oedema and orthostasis. Testing confirmed exogenous Cushing's syndrome and secondary adrenal insufficiency. Although ritonavir-fluticasone interactions have been previously reported as a cause for adrenal insufficiency, we propose that fluconazole increased the rapidity of onset and severity of symptoms through synergistic inhibition of the adrenal axis.
Int J STD AIDS 2012 May
PMID:Role of fluconazole in a case of rapid onset ritonavir and inhaled fluticasone-associated secondary adrenal insufficiency. 2264 97

Lipopolysaccharide (LPS), a potent stimulator of inflammatory responses in alveolar macrophages (AMs), activates several intracellular signaling pathways, including mitogen-activated protein kinases (MAPK). In the present study, we investigated the MAPK pathway in AMs of chronic bronchitis (CB) rats. CB was induced by endotracheal instillation of LPS followed by Bacillus Calmette Guerin injection through the caudal vein 1 week later. Specific inhibitors were used and protein phosphorylations were detected by Western blot. We found that Genistein (PTK inhibitor) could inhibit protein kinase C (PKC), phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt or PKB) MAPK signaling pathway with different degrees, LY294002 (PI3K inhibitor) could not only inhibit phospho-PI3K/Akt expression, but also inhibit p38 and c-Jun NH2-terminal kinases (JNK) phosphorylation. Calphostin C (PKC inhibitor) could inhibit phospho-PKC expression and exerted significant effects on extracellular signal-regulated kinases (ERK) phosphorylation, however, it had no impact on p38 and JNK phosphorylation. These results demonstrated that the LPS mediated signaling pathway of MAPK in AMs of CB rats could be described as follows: PTK-PI3K-Akt-JNK/p38 or PTK-PI3K-PKC-ERK, and PI3K may have a negative regulation on the activation of downstream proteins.
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PMID:Studies on mitogen-activated protein kinase signaling pathway in the alveolar macrophages of chronic bronchitis rats. 2546 75