PubMed Health⌕ Search

Biomedical subjects

E Philips

Publications and source records attributed to E Philips.

15 recordsLinked to original sources
PubMed2003

Treatment of urinary incontinence in cystic fibrosis.

BACKGROUND: Urinary incontinence (UI) is a newly recognised problem in cystic fibrosis. Whilst prevalence is well documented, there are no reports of assessment and treatment of the problem. METHODS: A previous study reports the prevalence of UI in women with CF to be 51/75 (68%). Nineteen women subsequently requested help for the problem and were referred to a physiotherapist specialising in women's health. A digital assessment was performed to measure pelvic floor muscle strength and endurance. An individualised programme of pelvic floor muscle exercises (PFME) was taught based on the assessment. A questionnaire addressed issues of assessment and treatment. RESULTS: 12 women were assessed. The median (range) age, FEV1% predicted and BMI were 20.9 (19.3-46.1) years, 45.9 (14.8-82.7) and 20.5 (16.1-26.0), respectively. The median strength of the pelvic floor muscle was moderate (Oxford Scale grade 3) with a hold time (endurance) of 5 s. At reassessment (median time 13.1 weeks), there was an improvement in endurance (P = 0.04), with no change in strength. This was supported by a subjective improvement in symptoms. Patients found the exercises were difficult to perform, difficult to fit into their treatment programme and adherence was poor. CONCLUSIONS: PFME are effective at improving endurance and reducing leakage over the short-term. Women are reluctant to be assessed and the CF team should provide support and encouragement with treatment. Long-term outcome and the mechanisms of UI in this group of patients need further evaluation.

Adolescent↗
PubMed2001

Effect of wortmannin on human eosinophil responses in vitro and on bronchial inflammation and airway hyperresponsiveness in Guinea pigs in vivo.

Many mediators activate eosinophils via transduction pathways involving the enzyme phosphatidylinositol 3-kinase. The initial investigation of wortmannin, a specific inhibitor of PI3-kinase, was of its effect on human and guinea pig eosinophil superoxide (O(2)(-)) release and degranulation in vitro. Subsequently, the effect on allergen- and Sephadex-induced bronchial inflammation and airway hyperresponsiveness (AHR) in vivo in guinea pigs was investigated. Wortmannin potently inhibited complement C5a-induced O(2)(-) generation and eosinophil peroxidase (EPO) release from human eosinophils, with 50% inhibition produced by a 1-10 nM concentration. Both aerosol allergen challenge of sensitized guinea pigs and intravenous injection of Sephadex beads in normal guinea pigs caused, in 24 h, significant eosinophilia and increased EPO activity in bronchoalveolar lavage fluid (BALF) and AHR to intravenous acetylcholine and histamine. In the allergic model, intranasal pretreatment with wortmannin had no effect on BALF eosinophilia, but dose dependently inhibited BALF EPO activity. At 1 mg/kg, the drug abolished the AHR to histamine, but not acetylcholine. In the Sephadex model, the drug significantly inhibited all three parameters (eosinophilia, increased EPO activity, and AHR to both spasmogens). These results show that wortmannin is a potent inhibitor of human eosinophil degranulation and that when administered intranasally can prevent AHR in allergen-challenged guinea pigs, probably by inhibiting eosinophil degranulation, but not their accumulation in BALF. This may be relevant to the possible clinical utility of wortmannin in conditions involving eosinophilic inflammation and AHR.

Administration, Intranasal↗
PubMed2000

Histamine H(2) receptors mediate the inhibitory effect of histamine on human eosinophil degranulation.

The effect of histamine on human eosinophil degranulation and the receptor mediating such effect were studied in vitro using the complement C5a-mediated eosinophil peroxidase (EPO) release model. Following pre-treatment with 5 microg ml(-1) cytochalasin B(CB), C5a induced a concentration-dependent release of EPO from eosinophils isolated from healthy donors. Histamine (0.1-50 microM), but not L-histidine, inhibited concentration-dependently C5a-induced EPO release with IC(50) (95% CI) of 0.6 microM (0.3-1.2 microM) and maximal inhibition of approximately 60%. A similar effect was seen with the selective H(2) agonists dimaprit (IC(50) (95% CI)=6.9 microM (3.2-10.6 microM)) and amthamine (IC(50) (95% CI)=0.4 microM (0.2-0.7 microM)). Neither the selective H(1) agonist 6-(2-(4-imidazolyl)ethylamino)-N-(4-trifluoromethylphenyl) heptanecarboxamide(HTMT), nor the selective H(3) agonists imetit (up to 100 microM) had any significant effect. The inhibition by histamine was reversed by cimetidine (0.1-30 microM) and other H(2) antagonists, but not the H(1) antagonist mepyramine (1.0- 100 microM), nor the H(3) antagonist thioperamide (1.0-100 microM). Cimetidine (1-30 microM) shifted to the right the dimaprit log dose-response curve, producing a pA(2) value of 5.9 and Schild's plot slope of 0.98, thus confirming simple competitive antagonism. Histamine (10-100 microM) increased intracellular level of adenosine 3',5'-cyclic monophosphate, which was completely abolished by cimetidine (30 microM), but not mepyramine or thioperamide. The cyclic AMP analogue - dibutyryl cyclic AMP - also inhibited degranulation (IC(50) approximately 300 microM). The cyclic AMP phosphodiesterase(PDE) IV inhibitor rolipram (10 microM) synergistically enhanced the inhibition of EPO release by histamine. These results suggest that histamine, via stimulation of H(2) receptors and a consequent elevation of intracellular levels of cyclic AMP, inhibits human eosinophil degranulation.

Adenylyl Cyclases↗
PubMed1999

Adenosine A3 receptors on human eosinophils mediate inhibition of degranulation and superoxide anion release.

The role of adenosine A3 receptors on human eosinophil degranulation and superoxide anion (O2-) release was studied in vitro using the complement fragment C5a as the main stimulus and employing a number of selective agonists and antagonists. In the presence of cytochalasin B (CB), C5a induced a dose-dependent release of the granular eosinophil peroxidase (EPO), but not O2-, whereas in the absence of CB O2- , but not EPO, was released. C5a-induced EPO release was inhibited dose-dependently by the selective A3 agonist N6-(3-iodobenzyl)-5'-N-methylcarbamoyladenosine (IB-MECA) and to a lesser extent by the less-selective N6-2-(4-amino-3-iodophenyl) ethyladenosine (APNEA). The IC50 (95% CI) for IB-MECA was 6.8 microM (3.1-12.0 microM). At concentrations up to 100 microM, neither adenosine nor the selective A1 agonist N-cyclopentyladenosine (CPA) and the selective A2 agonist 2-[[2-[4-(2-carboxyethyl)phenyl]ethyl]amino]-N-ethylcarboxamidoadenosine (CGS 21680) had any significant effect. The inhibitory effect of IB-MECA was almost completely abolished by pre-treatment with 1 microM of the selective A3 antagonist 9-chloro-2-(2-furyl)-5-phenylactylamino[1,2,4]triazolo[1,5-c]quina zoline (MRS 1220), but not the selective A1 antagonist 1,3-dipropyly-8-cyclopentylxanthine (DPCPX) or the selective A2 antagonist 3,7-dimethyl-1-propargylxanthine (DMPX). IB-MECA also significantly inhibited C5a-induced O2- release with IC50 (95% CI) of 9.5 microM (4.6-13.1 microM) whereas adenosine and the A1 agonist CPA potentiated this effect at low concentrations. The potentiation appeared to be a result of their direct O2- release from these cells, probably mediated via A1 receptors. The inhibition by IB-MECA was selectively reversed by MRS 1220. These results show that the A3 receptors on human eosinophils mediate inhibition of both degranulation and O2- release and suggest a therapeutic potential for A3 agonists in diseases such as asthma in which activated eosinophils are involved.

Cell Degranulation↗
PubMed1999

The classification of smile patterns.

Although "smile therapy" is still in its infancy, society has already placed a great demand on dentists to evaluate and treat smiles. The smile classification scheme and vocabulary presented in this article will aid in discussions between patient and dentist regarding esthetic treatment.

Classification↗
PubMed1999

The perfect gap: when are midline diastemas aesthetically acceptable?

To close or not close a midline diastema is a very significant issue. Ultimately, such decisions are subjective. The role of the dentist is to help patients understand the various fundamental geometric laws of aesthetics. When the relative balance and harmony of the distributed space are properly proportioned and conform to the laws of nature, either scenario is acceptable. Simple proportions using the Golden Rectangle can be used to help patients assess their individual choice.

Decision Support Techniques↗
PubMed1998

Family advocacy.

Explore the source record for details and available documents.

Consumer Advocacy↗
PubMed1978

Diagnostic value of the portable chest x-ray technic in pulmonary edema.

The ability of the portable chest x-ray film to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in thirty-seven observations of eleven patients. Ten of the eleven patients were suffering from acute respiratory failure. The radiologic assessment of the amount of pulmonary edema and the severity of left ventricular failure were compared with the physiologic shunt fraction, tracer-measured lung water, and pulmonary arterial wedge pressure. The radiologic scores for edema did not predict the shunt fraction or tracer measurements of lung water. The radiologic score for congestive failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the x-ray results were false-positive and 11 per cent false-negative. Results indicate that the portable chest x-ray technic does not provide quantitative information regarding cardiopulmonary function. It is especially hazardous to accept an x-ray diagnosis of congestive failure as the cause of pulmonary edema.

Adult↗
PubMed1978

Limitations of portable roentgenography of the chest in patients with acute respiratory failure.

The ability of the portable roentgenography of the chest to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in 37 observations of 11 patients. Ten of the 11 patients had acute respiratory failure. The roentgenologic assessment of the amount of pulmonary edema and the severity of left ventricular failure was compared with the physiologic shunt fraction, tracer measured lung water and the pulmonary arterial wedge pressure. The roentgenologic scores for edema did not predict the shunt fraction or tracer measured lung water. The roentgenologic score for congestive heart failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the roentgenograms were false-positive and 11 per cent were false-negative. Roentgenologic findings lagged behind physiologic derangements. Thus, the roentgenogram could predict the shunt value of the preceding day. Results indicate that it is hazardous to accept a portable roentgenographic diagnosis of congestive heart failure as a cause of pulmonary edema.

Acute Disease↗