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Bronchial

C.G. Smith et al., Tolerance develops to the disruptive effects of THC on the primate menstrual cycle, Science 219, 1453-1455, 1983. B.A. Mueller et al., Recreational drug use and the risk of primary infertility, Epidemiology 1, 195-200, 1990. A.J. Wilcox et al., Risk factors for early pregnancy loss, Epidemiology 1, 382-385, 1990. E.L. Abel, Marijuana and sex: A critical survey, Drug and Alcohol Dependence 8, 1-22, 1981. J.R.L. Ehrenkranz and W.C. Hembree, Effects of marijuana on male reproductive function, Psychiatric Annals 16, 243-249, 1986.
Ecp and epx levels are not related to bronchial hyperreactivity.
Cystic fibrosis CF ; , one of the most common and severe inherited diseases, is associated with defective fluid transport in various epithelia. The protein defective in CF is the Cl- permeable ion channel CFTR, the cystic fibrosis transmembrane conductance regulator, which is activated by cAMP-dependent phosphorylation 20 ; . CFTR channel opening and closing also requires the binding and hydrolysis of ATP at its two nucleotide binding domains 5, 23 ; . CFTR mutations in CF patients may impair channel gating, channel conductance, and or CFTR protein trafficking. Current therapeutic approaches for CF involve the control of chronic bacterial colonization in the airways and the improvement of mucus clearance. There is no therapy yet to treat the primary CF functional defect in vivo. However, several small organic compounds are able to increase CFTR Cl- conductance in vitro, such as the flavonoids apigenin and genistein 1, 13, 14, ; , the xanthines CPX and IBMX 10, 11, 25 ; , the substituted benzo[c]quinolizinium MPB-07 2 ; , and the benzimidazolone NS004 1, 9; see also for review refs. 12, 16, 22 ; . It is believed that selective and potent CFTR activators may be beneficial in CF to correct electrolyte fluid transport abnormalities. We recently used a lead-based combinatorial synthesis approach and high-throughput screening to identify a novel class of potent CFTR activators, the 7, 8-benzoflavones 7 ; . In a follow-up study, several isoxazoles and benzimidazolones were identified by a similar approach 17 ; . To assess the potency of these new compounds in native CFTR-expressing epithelia, we report short-circuit current measurements in primary human bronchial cell cultures. The best 7, 8-benzoflavone UCCF-029 ; and the best benzimidazolone UCCF-853 ; were characterized in their ability to activate Cl- conductance in combination with cAMP agonists and each other. An interesting observation was that the activating potency of these compounds depended on basal CFTR function phosphorylation state. Further studies of. 6. Glucocorticoids - Urbason average dose of 80 - 160 mg daily and cardiotonics; 7. Infusion therapy by drops venally according to the haemodynamic indications glucose and levulose solutions, Alvesin, alkaline solutions etc. ; 8. Cardiotonics - Strophanthin or digitalis preparations in ampoule form - parenterally. 9. Symptomatic medication - upon indications. Clinical model for acute poisonings by hydrogen sulphide - diagnostic antidote treatment method 1. Clinical characteristics 1.1. Catarrhal syndrome: irritation in the upper respiratory tract and the eyes, coughing, strangulation in the chest. 1.2. Pulmo-toxic syndrome: toxic lung oedema, bronchial spasm, early bronchopneumonia, acute respiratory insufficiency, apnoea. 1.3. Cerebral toxic syndrome: excitement, drowsiness, convulsions, coma. 1.4. Cardio-circulatory syndrome: shock state, acute lung heart at a later stage! ; . 1.5. Metabolite syndrome: severe acidosis of mixed type. 1.6. Paraclinical tests: roentgenogramme: spot shadows on both sides of the lungs; electrocardiogramme: dysrepolarization changes, arrhythmia, Ppulmonale. 2. Unified treatment programme 2.1. Respiratory reanimation: assisted or directed respiration after intratracheal intubation, oxygen inhalation. 2.2. Cardiovascular reanimation: cardiotonics, antishock and antiarrhythmic drugs. 2.3. Pulmoprotective drugs: broncholitics, diuretics, antibiotics. 2.4. Antidotes: 3% sodium bicarbonate solution, Becotid - aerosol mixture; antihypoxia drugs Nootropil Pyramem or Urbason doses ; or by means of antihypoxic methods. 2.5. Symptomatic treatment. Introduced over the years, with different pharmacokinetics, pharmakodynamics, potencies and bioavailabilities and more efficient delivery systems have been developed. [2, 14, 15]. Differences in pharmacokinetics determine the topical to systemic effect ratio or the pulmonary targeting of the drug. Differences in receptor-binding affinity, however, translate into differences in potency for different drugs. There is no method to evaluate the potency of inhaled GS in vivo. The standard screening test to determine the relative "potencies" for inhaled GS has been the McKenzie skinblanching test [5]. However, this procedure has come under criticism. The intensity of the blanching response to a GS varies from subject-to-subject and is influenced by ambient temperature and humidity and other factors [16]. The blanching effect score is difficult to compare among groups or among specific formulations conducted in different groups and the visual reading of the skin-blanching by the human eye is a subjective measure. Furthermore, the results are influenced by drug diffusibility through tissue, which is likely to vary in skin and in the airway. Most importantly, the test assesses vasoconstrictive efficacy rather than true potency receptor-binding affinity ; and may have little relevance to the anti-inflammatory effects of GS, which, in contrast to vasoconstriction, are mediated through genomic effects. Finally, aerosol delivery devices can produce clinically significant differences in topical activity by altering the dose deposited in the lung [17]. Alternative approaches are therefore desirable. The authors believe that the quantitative assessment of bronchial vasoconstriction, as described in this article, is such.
The ROADWATCH program was started in 1995 by a concerned group of citizens in the Town of Caledon, in partnership with police service, municipal government, health department and educators. The goal of the group was to reduce the number of fatalities and collisions on their local roads by changing driver attitudes and behaviours. ROADWATCH gives a community the opportunity to do something about dangerous aggressive driving by reporting information on such incidents on easy to use Citizen Report Forms. The program is promoted to teen drivers via secondary schools and to the community via media, road signs, and speaking engagements by volunteers. Completed citizen report forms are forwarded to the police via fax or community drop-off locations. Citizens who submit forms remain anonymous. The police then contact the plate owner via a three tiered response: First Citizen Reportletter to plated owner; Second Citizen Reportrepeat letter to plate owner and follow up phone call from police officer; Third Citizen Report third letter and personal visit from police officer. Charges may be laid. The forms are also used by the police to identify problem locations for repeated violations of dangerous aggressive driving behaviour. A traffic officer may direct specific enforcement projects on problem "hot spots". In addition to the education and engagement of the community for ROADWATCH, and enforcement by the police, ROADWATCH identifies problems with road design and or construction. Repeated violations at the same intersection or stretch of road have led to changes by the Public Works Department to decrease dangerous driving. Challenges of Peel's integrated approach include: The length of time it takes to build relationships and implement comprehensive, integrated interventions that address all partners' mandates; Sufficient funding to educate and mobilize the public and bumetanide. Summary of morphological areas scored for the bronchial E, baseline biopsy information. I, results of 6-month as described in "Materials and Methods, " and include. 26. Bloemen, P. G., M. C. van den Tweel, P. A. Henricks, F. Engels, M. J. van de Velde, F. J. Blomjous, and F. P. Nijkamp. 1996. Stimulation of both human bronchial epithelium and neutrophils is needed for maximal interactive adhesion. Am. J. Physiol. 270: L80L87. 27. Jagels, M. A., P. J. Daffern, B. L. Zuraw, and T. E. Hugli. 1999. Mechanisms and regulation of polymorphonuclear leukocyte and eosinophil adherence to human airway epithelial cells. Am. J. Respir. Cell Mol. Biol. 21: 418427. 28. Tosi, M. F., J. M. Stark, C. W. Smith, A. Hamedani, D. C. Gruenert, and M. D. Infeld. 1992. Induction of ICAM-1 expression on human airway epithelial cells by inflammatory cytokines: effects on neutrophil-epithelial cell adhesion. Am. J. Respir. Cell Mol. Biol. 7: 214221. 29. van der Velden, V. H. J., M. M. Verheggen, S. Bernasconi, S. Sozzani, B. A. Naber, C. A. J. van der Linden-van Beurden, H. C. Hoogsteden, A. Mantovani, and M. Versnel. 1998. Interleukin-1 and interferon- differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells. Eur. Cytokine Netw. 9: 269277. 30. Sousa, A. R., S. J. Lane, J. A. Nakhosteen, T. Yoshimura, T. H. Lee, and R. N. Poston. 1994. Increased expression of the monocyte chemoattractant protein-1 in bronchial tissue from asthmatic subjects. Am. J. Respir. Cell Mol. Biol. 10: 142147. 31. Alam, R., J. York, M. Boyars, S. Stafford, J. A. Grant, J. Lee, P. Forsythe, T. Sim, and N. Ida. 1996. Increased MCP-1, RANTES, and MIP-1 in bronchoalveolar lavage fluid of allergic asthmatic patients. Am. J. Respir. Crit. Care Med. 153: 13981404 and buprenorphine.

Bronchial pharmacy

Ably use fewer people and be more resilient to budget changes than the current force, which evolved during the era of large-scale sustained armored conflict. Also, our analysis indicates that military capabilities will drop rapidly with further decreases in the budget unless there is a substantial reengineering and reduction of infrastructure. In any case, debating the kinds of ideas displayed here would be useful. Our point is not that we know the answer, but rather that decisionmakers should be looking for the kinds of insights we offer notionally here. SOME PRELIMINARY SUBSTANTIVE OBSERVATIONS Having described our proposed framework and its methods, let us now share some preliminary results of using such analysis. Near- and Mid-Term Capabilities Against Rogue Nations For now, U.S. capabilities are very substantial, and U.S. forces will simply outclass any regional aggressor on the landscape. Indeed, our analysis of programmed future forces suggests the following: With sufficient warning time and reasonably effective allies, the United States should be able to defeat a classic armored invasion handily. In many cases, the United States should be able to handle two such invasions concurrently--so long as they are some weeks apart or, in some cases, even if they are more nearly simultaneous.7 Thus, classic armored invasions affecting U.S. interests "should be" obsolete. We will need to prepare for them indefinitely, so as to keep them obsolete. But they may not occur again, at least not in pure form as in the past and in our current plans.

Cost of Bronchial

H292 bronchial epithelial cells were seeded into 24-well dishes in RPMI 1640 10% fetal calf serum and grown to 7080% confluence. After serum starvation for 24 h, the cells were treated in serum-free medium with or without 10 ng ml tumor necrosis factor TNF ; - in the absence or presence of H 2O2 50400 M ; for 1, 3, or 4 h. the end of each time point, cells were lysed into SDS sample buffer and analyzed by SDS-PAGE and Western blotting with p85 PARP antibody and a pan PARP antibody, using previously described protocols 6 and buspirone. For example, the drug delivery regimen of the present invention is administered to treat a condition selected from the group consisting of vitamin and or mineral deficiency, cancer, addiction, arthritis, parkinson's disease, attention deficit disorder, cardiovascular disorder, cold flu symptoms, pain, childhood bronchial asthma, peptic ulcer, post-operative recuperation, and so forth as shown below.

Bronchial cost

During the course of 20 years of use of Isuprel brand of isoproDesdptioa: Isuprel brand of isoproterenol ; is available as: Solution 1: 200 in a buffered aqueous vehicle containing sodium terenol ; there has been no clinical evidence of teratogcnic effects. chloride, sodium citrate, and glycerin with chlorobutanol 0.5 per However, use of any drug in pregnancy, lactation, or in women of child-bearinn ane reauires that the wtential benefit of the drug be cent and sodium bisulfite 0.3 per cent as preservatives. possible hazards-to the mother or child. Solution 1: 100 in a buffered aqueous vehicle containing sodium weighed --its chloride, sodium citrate, citric acid, and saccharin with chlorobu- Advene Reaciioim Tachycardia, palpitation, nervousness, nausea, tan01 0.5 per cent and sodium bisulfite 0.3 per cent as preservatives. and vomiting may occur from overdosage. Rarely, do Co~~lrahdIcation: e of isoproterenol in patients with preexisting flushing of the skin, tremor, dizziness, weakness, sweating, prccordlal U s cardiac arrhythmias associated with tachycardia is generally con- distress, or anginal-type pain occur. The inhalation route is u s sidered contraindicated because the cardiac stimulant effect of the accompanied by a minimum of side effects. These untoward w o n disappear quickly and do n t rul9 inwnveniencc the patient o, drug may aggravate such disorders. W r i Excessive use of an adrenergic aerosol should be dis- to the extent that the drug must be dsontmued. No cumulative a no couraged as it may lose its effectiveness. effects have been reported. Occasional patients have been reported to develop severe para- Dosage aud AddnMdbm: Bronchial Asthma-Oral Inhalation: doxical airway resistance with repeated, excessive use of isopro- Solution 1: 200 and 1: 100- For adults a$ children, the 1: 200 soluterenol inhalation preparations. The cause of this refractory state is tion is ad htqrcd by lynd-bulb nebullzahon in a dosap of 5 to unknown. It is advisable that in such instances the use of this prepara- 15 deep ~nhalahons usmg an all glass or p h mbuhcr ; , retion be discontinued immediately and alternative therapy instituted, peated if necessary in 10 to minutes. In time, the patient can adsince in the reported cases the patients did not respond to other forms just the dosage. When oxygen aerosolization is used, up to 0.5 d of the 1: 200 solution is administered with the oxygen flow adjusted of thera untd the drug was withdrawn. Deaths E v e been reported following excessive use of isoproterenol to 4 liters per minute over a period of 15 to minutea. inhalation prepadoxu and the exact cause is unknown. Cardiac ar- The 1: 100 solution should be used if a stronger solution seems to be indicated. The dose bv hand-bulb nebulization is 3 to deep inhalarest waa notedin several inatanas. ~~Epinephrine should not be administered with Isuprel, tions; by oxygen ae&lization, up to 0.3 ml. brand of isoproterenol, as both drugs are direct mdiac stimulants Emphysema, Chronic Bronchitis: Oral inhalation doses are the name and thdr combined effects may induce serious arrhythmia. If de- as forasthma, repeated three or four times daily. sired they may, however, be alternated, provided an interval of at H &~ppllcd: Inhalation and Aerosolization: Solution I: 200, o For bottles of 10 and 50 ml.-Solution 1: 100, bottles of 10 d least four hours has elapsed. Isoproterenol should be used with caution in patients with d o vascular disorders including coronary insufficiency, diabetes, or hypathyroidim, and in persons sensitive to sympathomimetic Wi~lthrw LaboratoriesNew Y r , .Y.10016 o kN and busulfan. For those mothers who are pregnant but not receiving ART, the MoH has already drawn up guidelines on the prevention of the mother from transmitting HIV to her child. The country is already implementing a PMTCT program at many sites using Nevirapine or Zidovudine as single drug intervention Table 10 ; . Table 10: Recommended Regimens for PMTCT Intervention. Target Nevirapine NVP ; Zidovudine ZDV ; Mother 200 mg stat at the 300 mg twice daily for at least beginning of labor or 4 weeks before delivery then latest 30 minutes before 300 mg every 3 hrs during delivery labor then 300 mg twice daily for 1 week after delivery Infant Within 72 Syrup 2 mg kg stat Syrup 5 mg kg twice daily for one hours of birth ; week For more information please contact MoH or see PMTCT National Guidelines.
1. Wierenga, E. A., M. Snoek, C. de Groot, I. Chretien, J. D. Bos, H. M. Jansen, and M. L. Kapsenberg. 1990. Evidence for compartmentalization of functional subsets of CD4 T lymphocytes in atopic patients. J. Immunol. 144: 4651. 2. Parronchi, P., D. Macchia, M.-P. Piccinni, P. Biswas, C. Simonelli, E. Maggi, M. Ricci, A. A. Ansari, and S. Romagnani. 1991. Allergen- and bacterial antigenspecific T-cell clones established from atopic donors show a different profile of cytokine production. Proc. Natl. Acad. Sci. USA 88: 4538. 3. Hamid, Q., M. Azzawi, S. Ying, R. Moqbel, A. J. Wardlaw, C. J. Corrigan, B. Bradley, S. R. Durham, J. V. Collins, P. K. Jeffrey, D. J. Quint, and A. B. Kay. 1991. Expression of mRNA for Interleukin-5 in mucosal bronchial biopsies from asthma. J. Clin. Invest. 87: 1541. 4. Del Prete, G. F., E. Maggi, P. Parronchi, I. Chretien, A. Tiri, D. Macchia, M. Ricci, J. Banchereau, J. E. de Vries, and S. Romagnani. 1988. IL-4 is an essential factor for the IgE synthesis induced in vitro by human T cell clones and their supernatants. J. Immunol. 140: 4193. 5. Pene, J., F. Rousset, F. Briere, I. Chretien, J. Y. Bonnefoy, H. Spits, T. Yokota, N. Arai, K. Arai, J. Banchereau, and J. E. de Vries. 1988. IgE production by normal human lymphocytes is induced by interleukin-4 and suppressed by interferons and and prostaglandin E2. Proc. Natl. Acad. Sci. USA 85: 6880. 6. Punnonen, J., G. Aversa, B. G. Cocks, A. N. J. MacKenzie, S. Menon, G. Zurawski, R. de Waal Malefyt, and J. E. de Vries. 1993. Interleukin 13 induces interleukin 4-independent IgG4 and IgE synthesis and CD23 expression by human B cells. Proc. Natl. Acad. Sci. USA 90: 3730. 7. Thompson-Snipes, L., V. Dhar, M. W. Bond, T. R. Mosmann, K. W. Moore, and D. M. Rennick. 1991. Interleukin-10: a novel stimulatory factor for mast cells and their progenitors. J. Exp. Med. 173: 507. 8. Kitamura, Y., T. Kasugai, N. Arizono, and H. Matsuda. 1993. Development of mast cells and basophils: processes and regulation mechanisms. Am. J. Med. Sci. 306: 185. 9. Sanderson, C. J., D. J. Warren, and M. Strath. 1985. Identification of a lymphokine that stimulates eosinophil differentiation in vitro: its relationship to interleukin 3, and functional properties of eosinophils produced in cultures. J. Exp. Med. 162: 60. 10. Yamaguchi, Y., Y. Hayashi, Y. Sugama, Y. Miura, T. Kasahara, S. Kitamura, M. Torisu, S. Mita, A. Tominaga, and K. Takatsu. 1988. Highly purified murine interleukin 5 IL-5 ; stimulates eosinophil function and prolongs in vitro survival: IL-5 as an eosinophil chemotactic factor. J. Exp. Med. 167: 1737. 11. Romagnani, S. 1994. Regulation of the development of type 2 T-helper cells in allergy. Curr. Opin. Immunol. 6: 838. 12. Sato, Y., M. Roman, H. Tighe, D. Lee, M. Corr, M.-D. Nguyen, G. J. Silverman, M. Lotz, D. A. Carson, and E. Raz. 1996. Immunostimulatory DNA sequences necessary for effective intradermal gene immunization. Science 73: 352. 13. Raz, E., E. Tighe, Y. Sato, M. Corr, J. A. Dudler, M. Roman, S. L. Swain, H. L. Spiegelberg, and D. A. Carson. 1996. Preferential induction of a Th1 immune response and inhibition of specific IgE antibody formation by plasmid DNA immunization. Proc. Natl. Acad. Sci. USA 93: 5141. 14. Hsu, C. H., K. Y. Chua, M. H. Tao, S. K. Huang, and K. H. Hsieh. 1996. Inhibition of specific IgE response in vivo by allergen-gene transfer. Int. Immunol. 8: 1405. 15. Spiegelberg, H. L., E. M. Orozco, M. Roman, and E. Raz. 1997. DNA immunization: a novel approach to allergen-specific immunotherapy. Allergy 52: 964. 16. Klinman, D. M., A.-K. Yi, S. L. Beaucage, J. Conover and A. M. Krieg. 1996. CpG motifs present in bacterial DNA rapidly induce lymphocytes to secrete interleukin 6, interleukin 12, and interferon . Proc. Natl. Acad. Sci. USA 93: 2879. 17. Krieg, A. M., L. Love-Homan, A-K. Yi, and J. T. Harty. 1998. CpG DNA induces sustained IL-12 expression in vivo and resistance to Listeria monocytogenes challenge. J. Immunol. 161: 2428. 18. Roman, M., E. Martin-Orozco, J. S. Goodman, M. D. Nguyen, Y. Sato, A. Ronaghy, R. S. Kornbluth, D. D. Richman, D. A. Carson, and E. Raz. 1997 and butorphanol. Pseudoephedrine directly stimulates alpha-adrenergic receptors of respiratory mucosa causing vasoconstriction; directly stimulates beta-adrenergic receptors causing bronchial relaxation, increased heart rate and contractility!
The overall 5-year survival rate is approximately 12% 2 ; . Given the poor outcome in patients with advanced disease, recent efforts have focused on the reversal of bronchial premalignancy. However, interventions made thus far in individuals at increased risk of developing lung cancer have revealed no benefit 3 ; . Effectively reversing bronchial premalignancy will require that we identify the critical genetic and biochemical events that cause malignant progression in the bronchial epithelium. Activation of the PI3K pathway causes malignant transformation in vitro and is sufficient to induce a variety of solid tumors in mouse models of human cancer 4 8 ; . Factors contributing to PI3K pathway activation in cancer include alterations in the PI3K p85 regulatory subunit or the p110 catalytic subunit, PTEN, and AKT also known as protein kinase B ; , which is a downstream effector molecule of the PI3K pathway. AKT is activated by the PI3K phospholipids PI-3, 4, 5-P3 and PI-3, 4-P2, which bind to the pleckstrin homology domains of AKT and anchor it to the plasma membrane. In addition, the PI3K-dependent kinases phosphoinositide-dependent kinase and integrin-linked kinase activate AKT by phosphorylating it at Thr308 and Ser473, respectively 9, 10 ; . AKT activation is required for the transforming effects of PI3K 11 ; . Previous studies have reported increased expression of p-AKT Ser473 ; in NSCLC 1217 ; , providing evidence of AKT activation in fully transformed bronchial epithelium. However, it is not clear when AKT is activated during the process of malignant progression. Here we examined p-AKT Ser473 ; expression in normal bronchial epithelium, "reactive" epithelium bronchial hyperplasia and squamous metaplasia ; , early bronchial neoplasia bronchial dysplasia ; , and NSCLC. We found p-AKT Ser473 ; expression in a strikingly high percentage of bronchial dysplasia specimens, supporting PI3K pathway activation as an early event in lung tumorigenesis. Materials and Methods Tissue Specimens. We evaluated 44 normal bronchoscopic biopsy specimens and 9 specimens considered to have reactive histology hyperplasia or squamous metaplasia ; obtained at baseline from 20 former smokers who had at least a 20-packyear smoking history and no evidence of cancer at the time of bronchoscopic examination.4 We also evaluated 25 bronchoscopic biopsy specimens with dysplastic features obtained from 25 smokers who had at least a 30-pack-year smoking history and morphometric evidence of dysplasia in sputum samples 18 ; and 76 NSCLC specimens resected from 76 patients. Pathological staging of NSCLC specimens was based on op and byetta. AIRWAY MUCUS AND EFFECT OF LIQUID SECRETION INHIBITION 8. Boucher, R. C. Human airway ion transport. Am. J. Respir. Crit. Care Med. 150: 581593, 1994. Colten, H. R. Cystic fibrosis. In: Harrison's Principles of Internal Medicine 12th ed. ; , edited by J. D. Wilson, E. Braunwald, K. J. Isselbacker, R. G. Petersdorf, J. B. Martin, A. S. Fauci, and R. K. Root. New York: McGraw-Hill, 1991, p. 10721074. 10. Dasgupta, B., and M. King. Molecular basis for mucolytic therapy. Can. Respir. J. 2: 223230, 1995. Engelhardt, J. F., J. R. Yankaskas, S. T. Ernst, Y. Yang, C. R. Marino, R. C. Boucher, J. A. Cohn, and J. M. Wilson. Submucosal glands are the predominant site of CFTR expression in the human bronchus. Nat. Genet. 2: 240248, 1992. Galabert, C., J. Jacquot, J. M. Zahn, and E. Puchelle. Relationship between the lipid content and the rheological properties of airway secretions in cystic fibrosis. Clin. Chim. Acta 164: 139149, 1987. Girod, S., C. Galabert, A. Lecuire, J. M. Zahm, and E. Puchelle. Phospholipid composition and surface-active properties of tracheobronchial secretions from patients with cystic fibrosis and chronic obstructive pulmonary disease. Pediatr. Pulmonol. 13: 2227, 1992. Hogan, D. L., D. L. Crombie, J. I. Isenberg, P. Svendsen, O. B. Schaffalitzky de Muckadell, and M. A. Ainsworth. CFTR mediates cAMP- and Ca2 -activated duodenal epithelial HCO3 secretion. Am. J. Physiol. 272 Gastroinest. Liver Physiol. 35 ; : G872G878, 1997. 15. Inglis, S. K., M. R. Corboz, and S. T. Ballard. Effect of Cl and HCO3 transport blockers on submucosal gland duct mucin content in acetylcholine-treated bronchi Abstract ; . Pediatr. Pulmonol. Suppl. 14: 232, 1997. Inglis, S. K., M. R. Corboz, A. E. Taylor, and S. T. Ballard. Regulation of ion transport across porcine distal bronchi. Am. J. Physiol. 270 Lung Cell. Mol. Physiol. 14 ; : L289L297, 1996. 17. Inglis, S. K., M. R. Corboz, A. E. Taylor, and S. T. Ballard. Effect of anion secretion inhibition on mucus secretion by airway submucosal glands. Am. J. Physiol. 272 Lung Cell. Mol. Physiol. 16 ; : L372L377, 1997. 18. Inglis, S. K., M. R. Corboz, L. Trout, A. E. Taylor, and S. T. Ballard. Effect of HCO3 secretion inhibitors on acetylcholineinduced PD and glandular mucin content in distal bronchi Abstract ; . FASEB J. 3: A562, 1997. 19. Jacquot, J. E., E. Puchelle, J. Hinnrasky, C. Fuchey, C. Bettinger, C. Spilmont, N. Bonnet, A. Dieterle, D. Dreyer, A. Pavirani, and W. Dalemans. Localization of the cystic fibrosis transmembrane conductance regulator in airway secretory glands. Eur. Respir. J. 6: 169176, 1993. Jiang, C., W. E. Finkbeiner, J. H. Widdicombe, P. B. McCray, and S. S. Miller. Altered fluid transport across airway epithelium in cystic fibrosis. Science 262: 424427, 1993. Jiang, C., W. E. Finkbeiner, J. H. Widdicombe, and S. S. Miller. Fluid transport across cultures of human tracheal glands is altered in cystic fibrosis. J. Physiol. Lond. ; 501: 637647, 1997. Kartner, N., J. W. Hanrahan, T. J. Jensen, A. L. Naismith, S. Sun, C. A. Ackerley, E. F. Reyes, L.-C. Tsui, J. M. Rommens, C. E. Bear, and J. M. Riordan. Expression of the cystic fibrosis gene in non-epithelial invertebrate cells produces a regulated anion conductance. Cell 64: 681691, 1991. King, M. Relationship between mucus viscoelasticity and ciliary transport in guaran gel frog palate model system. Biorheology 17: 249254, 1980. King, M. Is cystic fibrosis mucus abnormal? Pediatr. Pulmonol. 15: 120122, 1981. King, M. Role of mucus viscoelasticity in cough clearance. Biorheology 24: 589597, 1987. King, M. Magnetic microrheometer. In: Methods in Bronchial Mucology, edited by P. C. Braga and L. Allegra. New York: Raven, 1988, p. 7383 and bronchial.

Orrin Devinsky, M.D., from the NYU Medical Center's and campral.

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