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P Herman

Publications and source records attributed to P Herman.

At least 91 records · Page 5Linked to original sources

Glucocorticosteroids increase sodium transport in middle ear epithelium.

The effect of glucocorticosteroids on ion transport was investigated on a middle ear cell line with the short-circuit current (Isc) technique. Dexamethasone (DXM) produced a dose- and time-dependent increase in Isc. Concentration of half-maximal stimulation was 2.68 x 10(-8) M. This effect was blunted by the glucocorticoid antagonist RU-38486 and was related to Na+ transport, as evidenced by the inhibition induced by 1) apical addition of the Na+ channel inhibitor benzamil (10(-6) M) or 2) substitution of Na+ with N-methylglucamine in the incubation medium. The increase in Na+ transport resulted from a primary modulation of apical Na+ entry, since 1) the Na(+)-K(+)-ATPase activity of cellular homogenates was not modified by corticosteroids and 2) the DXM-induced increase in the ouabain-sensitive uptake of 86Rb was blunted by benzamil. Ribonuclease protection assay revealed 1) a constitutive expression of the mRNA encoding the alpha-subunit of the epithelial Na+ channel and 2) that DXM increased the expression of this transcript. This increase was dose dependent and paralleled changes in transepithelial Na+ transport. This study suggests that a component of the beneficial effect of steroid therapy for the treatment of otitis media might be related to increased fluid clearance.

Adenosine Triphosphate↗

Modulation of middle ear epithelial function by steroids: clinical relevance.

The efficacy of steroid therapy for the treatment of otitis media in children remains controversial, and a putative modulation of the middle ear epithelial function has to be demonstrated. Using the MESV cell line, short-circuit current (ISC) technique was used to evaluate changes in ion transport induced by glucocorticoids. Dexamethasone (DXM) produced a dose- and time-dependent increase in ISC in MESV cells. This effect was inhibited by specific glucocorticoid antagonist (RU-38486) and was related to a sodium transport, since the DXM-induced increase in ISC could be prevented or abolished i) by apical addition of the specific Na+ channel inhibitor benzamil; or ii) by substitution of sodium with N-Methyl-glucamine in the incubation medium. RNase protection assay revealed that DXM increased the expression of the alpha subunit sodium channel mRNA, which changes paralleled the modulation of ion transport. These data demonstrate that steroids up-regulate the trans-epithelial sodium transport in the middle ear epithelium. As far as these experimental data can be extrapolated to the in vivo situation, a component of the beneficial effect of steroid therapy for the treatment of otitis media may result from a corticosteroid-induced improvement in fluid clearance from the middle ear.

Amiloride↗

[Rotatory impulse test does not replace caloric tests].

We sought to determine whether the rotatory impulsional test was capable of exploring the canalar function with sufficient precision to replace the caloric test, as it has been recently affirmed. We first compared the observed preponderance from this test with that measured during a sinusoidal (20 and 4 s) test. We observed that, in the case of a significant preponderance for a given test, there was complete redondance with the preponderance observed with any other test. The rotatory impulsional test does not present any specific advantage compared to other kinetic test as far as the observation of the preponderance phenomenon. We then compared the preponderance with the results of the caloric tests and came to the following conclusions i) the absence of preponderance does not allow us to predict the absence of vestibular deficit, due to the fact that 37% of the deficits were compensated for including acoustic neuroma; ii) the presence of a preponderance does not allow a priori to say whether it is of vestibular, cervical, or central origin and systematic caloric tests shows that almost one fourth of preponderance observed is not associated with unilateral weakness iii) supposing that a clinical argument allow us to conclude as to the probable vestibular origin of a vestibular preponderance, the direction of this preponderance does not allow us to determine which side is involved. In fact, if the undercompensated deficits are 3 times more frequent than overcompensated deficits, the proportion of preponderance not linked to a significant deficit indicates that the probability of encountering a preponderance related to a specific undercompensated deficit is approximately 50%. We thus did not find in the rotatory impulsional test any specific advantage allowing us to predict the laterality of a vestibular lesion.

Caloric Tests↗

[Therapeutic management of craniocervical chordoma].

Chordomas are rare neoplasms of notochordal origin that arise along the vertebral axis. In the cervicofacial area, they show a marked proclivity for the sphenooccipital region. These slow-growing and infiltrating tumors are often discovered because of neglected symptoms related to the ENT field such as nasal obstruction, snoring, dyspnea or dysphagia in the case of anterior development, serous otitis media, cervical pain, or even palsy of the X, XI, or XII cranial nerves when the tumor develops toward the foramen jugulare or the foramen magnum. Prognosis is usually poor because of local malignancy, proximity to critical central nervous system structures, and volume of the tumor. Surgery is the preferred treatment for these extradural tumors, but most authors recommend postoperative irradiation because of surgical spillage or residual tumor. However, conventional irradiation is limited by the sensitivity of surrounding structures, which results in a poor rate of local control. We present 9 cases of histologically proven diagnosis of chordoma treated from 1984 to 1994 at our institution. Prognosis and therapeutic modalities are discussed. Therapeutic improvement might be brought the protontherapie, which ensures a better local control, and therefore may transform the prognosis of the disease.

Adolescent↗

Traumatic luxation of the stapes evidenced by high-resolution CT.

We encountered a case of acquired perilymphatic fistula in which the origin of the disease, namely, the stapes begin medially displaced into the vestibule, was shown by thin-section CT. Accordingly, we recommend that every patient with suspected perilymphatic fistula of traumatic origin undergo high-resolution CT of the petrous bone.

Female↗

Splenic abscess.

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Abdominal Abscess↗

Evidence for Na-K-Cl cotransport in alveolar epithelial cells: effect of phorbol ester and osmotic stress.

We have investigated the presence of Na-K-Cl cotransport in alveolar type II cells using uptake of 86Rb. Several data support the presence of a Na-K-Cl cotransport in these cells. First, a large fraction of ouabain-resistant 86Rb uptake was inhibited by bumetanide and furosemide. Second, bumetanide-sensitive 86Rb uptake required the presence of Na+ and Cl- in the incubation medium; dependency on extracellular Na+ and K+ was hyperbolic, with a Km of 14.6 mM and 8.3 mM, respectively, while dependency on extracellular Cl- was sigmoidal, which suggests a 1:1:2 stoichiometry. Third, a fraction of amiloride-insensitive 22Na influx was deeply inhibited by bumetanide. 22Na influx was dependent on the presence of extracellular K+ and Cl-. Since Na-K-Cl activity dramatically decreased with time in culture, further characterization of the cotransport on polarized cells could not be performed. The phorbol ester PMA inhibited Na-K-Cl cotransport in a time- and concentration-dependent manner. This inhibition was mimicked by oleoylacetylglycerol, dioctanoylglycerol, and the diacylglycerol kinase inhibitor R59022, and was reversed by an antagonist of PKC, staurosporine. Since the Na-K-Cl cotransport has been reported to be involved in cell volume regulation, we investigated its modulation by changes in extracellular osmolarity. Na-K-Cl activity was increased after a two-step procedure: swelling in hypotonic medium followed by shrinking in hypertonic medium. Under these conditions, cotransport activity increased whenever PKC activity was up- or downregulated, which suggests that the cell volume-induced modulation of the cotransport is independent from the PKC activity. Though we were not able to determine the polarity of the cotransport, it may also be involved in the absorptive function of alveolar type II cells, and would provide an alternate pathway for sodium entry.

Animals↗

Luminal non-selective cation and outwardly rectifying chloride channels in cultured strial marginal cells from gerbil.

Ionic channels located on the luminal side of strial marginal cells (MCs) of gerbil in culture were investigated using the patch-clamp technique. Two types of channels were identified. The most frequently recorded single-channel activity corresponded to a non-selective cation (NSC) channel with a conductance of 23.7 +/- 0.2 pS (n = 18) in symmetrical NaCl conditions. The channel was activated by internal Ca2+ and inhibited by internal adenine nucleotides and flufenamic acid. Spontaneous activity of NSC channels was found in 16% of the cell-attached patches and with a very high density (9 +/- 2 levels/patch, n = 28) in 100% of the excised patches. An outwardly rectifying chloride (ORC) channel was also identified in 14% of the patches but only after excision. The channel exhibited at 0 mV a unit conductance of 26.8 +/- 1.3 pS (n = 8) and a strong outward rectification in symmetrical NaCl conditions, and the open probability increased with depolarization. The luminal NSC channel and the ORC channel evidenced in this study might participate in the production of endolymph. Although extrapolation of the presents results to the in vivo situation should be made with caution, this study suggests that culture of strial MCs may be a suitable model for investigation of endolymph physiology.

Adenine Nucleotides↗

Oxygen metabolites modulate sodium transport in gerbil middle ear epithelium: involvement of PGE2.

The middle ear epithelium and respiratory epithelia share basic properties such as homeostasis of air-filled cavities and mucociliary clearance toward the pharynx. With the middle ear SV40-transformed (MESV) cell line, we used the short-circuit current (Isc) technique to investigate changes in ion transport induced by oxidants. Xanthine and xanthine oxidase on the basal side of the monolayers dramatically increased Isc up to 50%. This effect was not affected by superoxide dismutase or mannitol, but could be blunted by catalase or 1,3-dimethyl-2-thiourea. Increasing concentrations of H2O2 from 10(-5) to 5 x 10(-4) M produced a dose-dependent increase in Isc from 0.26 +/- 0.16 up to 4.21 +/- 0.43 microA/cm2 (P < 0.05, n = 5). Concentration of half-maximal stimulation (EC50) was 4.68 x 10(-5) M. This effect was inhibited by indomethacin and was related to a sodium transport, since the H2O2-induced increase in Isc could be prevented or abolished by 1) apical addition of benzamil (10(-6)M) and 2) substitution of sodium with N-methyl-glucamine. H2O2 exposure also induced indomethacin-sensitive increase in released prostaglandin (PG) E2 (EC50 = 5.62 x 10(-5) M) and in cAMP content (EC50 = 3.95 x 10(-5) M) with similar kinetics. These results suggest that exposure of MESV cells to oxidants stimulates the production of PGE2, which in turn increases the transepithelial sodium transport rate.

Animals↗

Stimulation of sodium transport by oxidants in middle ear epithelium in primary culture.

Primary cultures of middle ear (ME) epithelial cells from gerbils were used to investigate the effect on ion transport of reactive oxygen species (ROS), which are major inflammatory mediators. Short-circuit current measurements revealed an unexpected result: low concentrations of ROS induced an increase in transepithelial sodium transport. This stimulation was mediated by the endogenous synthesis of prostaglandin E2, which in turn increased the intracellular adenosine 3',5'-cyclic monophosphate (cAMP) content. This effect was blunted by indomethacin. By stimulating sodium and fluid transport, ROS may reduce the depth of the periciliary fluid layer, and may thus be involved in the impairment of mucociliary clearance which initiates chronic otitis media.

Adenine Nucleotides↗