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Biomedical subjects

T Troost

Publications and source records attributed to T Troost.

10 recordsLinked to original sources
PubMed2000

Unilateral true vocal fold paralysis: cause of right-sided lesions.

At the Georgetown University Center for the Voice, 778 patients were referred for evaluation between July 1, 1990, and June 30, 1995. During this 5-year period, right true vocal fold paralysis or paresis was diagnosed in 24 of these patients (3%). Videostroboscopy, voice analysis, and patient records were reviewed. Ages ranged from 23 to 80 years, and sex distribution approximated a 1:1 ratio. The patients presenting symptoms included hoarseness, dysphagia, choking, voice pitch change, voice weakness, fatigability, and breathiness. Sources of the vocal fold dysfunction included iatrogenic, traumatic, central, and infectious causes.

Adult↗
PubMed1998

Glucocorticoids decrease c-fos expression in human nasal polyps in vivo.

BACKGROUND: Activated c-fos binds to jun proteins to form the activation protein 1 (AP-1) transcription factor that regulates cytokine and other proinflammatory genes. c-Fos may play a key role in nasal polyp formation. Glucocorticoids may exert their anti-inflammatory effects through an interaction of glucocorticoid receptors with AP-1 that leads to mutual inactivation of both factors, and a "default" termination of AP-1 mediated gene activation. This may explain the beneficial effects of glucocorticoids in the treatment of nasal polyps. METHODS: To test this hypothesis in humans in vivo the immunohistochemical expression of c-fos-immunoreactive material (c-fos-irm) was assessed in nasal polyps from eight steroid naive subjects, polyps from eight subjects treated with topical beclomethasone dipropionate (BDP), and normal inferior turbinate nasal mucosa (n = 6). RESULTS: mRNA for c-fos was detected in all nasal polyps and normal mucosa. In contrast, c-fos-irm was present in all steroid naive subjects but in only two of the eight subjects treated with BDP (p = 0.007, two-tailed Fisher's exact test). c-Fos-irm was expressed solely in epithelial cells and glandular structures; it was expressed in normal epithelium and glands, but the staining intensity was low. CONCLUSION: Glucocorticoids appear to modulate expression of c-fos-irm and possibly AP-1 in human airway epithelial cells in vivo.

Adult↗
PubMed1997

Glucocorticoids induce beta2-adrenergic receptor function in human nasal mucosa.

Glucocorticoids are hypothesized to induce beta2-adrenergic receptors (beta2-R) and their functions. The ability of dexamethasone (DEX) in vitro and beclomethasone dipropionate (BDP) in vivo to induce beta2-R messenger RNA (mRNA) and function was investigated in human nasal mucosa. In this tissue, albuterol does not stimulate exocytosis either in vivo or in vitro (Mullol and coworkers, 1992). Therefore, induction of beta2-R-mediated glandular exocytosis by glucocorticoids was proposed as an unambiguous outcome measure. Human nasal mucosa was cultured for 3 d with and without 1 microM DEX, then challenged with media or 100 microM albuterol. Culture supernatants were collected for measurement of exocytosed glandular products. Explant mRNA was extracted for reverse transcriptase-polymerase chain reaction (RT-PCR), and in situ hybridization of beta2-R mRNA performed. In vivo, normal subjects received saline or BDP for 3 d before albuterol nasal provocation. Concentrations of exocytosed products were measured in nasal secretions. RNA was extracted from nasal epithelial scrapings for RT-PCR. In vitro, DEX treatment induced albuterol-mediated glandular exocytosis (p < 0.04), and increased the steady-state beta2-R/beta-actin mRNA ratio (p < 0.05), and expression of beta2-R mRNA in glands. In vivo, BDP increased the beta2-R/beta-actin mRNA ratio in epithelial scrapings (p < 0.04), but did not induce albuterol-mediated glandular secretion. We conclude that glucocorticoids increase steady-state beta2-R mRNA levels in vivo and in vitro, and can induce beta2-R function as assessed by submucosal gland exocytosis in vitro. While topical BDP induced epithelial beta2-R mRNA, it did not modulate exocytosis from the deeper submucosal glands.

Administration, Topical↗
PubMed1995

Jet stylets as an aid for replacement of tracheostomy tubes.

Difficulty in tracheostomy tube replacement can be life-threatening in a patient who is dependent on the tracheostomy for ventilation. The use of jet styles for tracheostomy tube replacement in these patients facilitates the tube exchange and allows for jet ventilation if any difficulty is encountered during the tube replacement. We describe two cases in which jet stylets proved to be helpful during tracheostomy tube replacement and discuss considerations that are important for the safe use of these devices.

Aged↗
PubMed1991

Submandibular sialadenitis presenting as Ludwig's angina.

Previous descriptions of Ludwig's angina have focused on the odontogenic etiology and the absence of gland involvement. Incision and drainage of the involved fascial spaces without excision of the submandibular gland has traditionally been the recommended surgical treatment. Two case reports of edentulous patients illustrate acute submandibular sialadenitis spreading onto the fascial spaces described in association with Ludwig's angina. Surgical procedures included incision and drainage, along with excision of the submandibular gland. In select cases clinically resembling Ludwig's angina where submandibular sialadenitis is the etiology, we advocate that gland excision be included with a definitive incision and drainage procedure.

Aged↗
PubMed1979

Phenoxazinone biosynthesis: accumulation of a precursor, 4-methyl-3-hydroxyanthranilic acid, by mutants of Streptomyces parvulus.

Mutants of Streptomyces parvulus that are blocked in the synthesis of the phenoxazinone-containing antibiotic, actinomycin, were isolated by the 'agar piece' method (after ultraviolet irradiation or treatment with 8-methoxypsoralen plus near-ultraviolet light). Radiolabelling experiments in conjunction with paper, thin-layer and column chromatography revealed that 4-methyl-3-hydroxyanthranilic acid (MHA) is a major metabolite accumulated by these mutants. Studies in vitro and in vivo provided evidence that MHA is a precursor of the phenoxazinone chromophore, actinocin. Normally MHA does not accumulate during growth or antibiotic synthesis by the parental strains. Protoplasts derived from the mutant strain AM5 synthesized MHA in significant amounts. A scheme is proposed for the biosynthesis of actinomycin D that accounts for the accumulation of MHA by the mutants.

3-Hydroxyanthranilic Acid↗