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A new bicycle advocacy group has formed in the Greater Hartford area to promote bicycling in Central Connecticut. The Central Connecticut Bicycle Alliance CCBA ; has been formed by a group of area bicyclists as a non-profit organization that will work to: Promote bicycling as an environmentally friendly, healthy and economical form of transportation and recreation, improve the bicycling environment and the quality of life in the Central Connecticut Region, and educate motorists and bicyclists about their respective rights and responsibilities. The CCBA is an outgrowth of the Capitol Region Bike to Work Committee, a project of the Capitol Regional Council of Governments CRCOG ; . For those interested in learning more about the CCBA or in becoming a member, visit wecyclect.
A coalition of disability rights organizations has announced the launch of ADA WATCH , an Internet site designed to defend and strengthen the implementation of the ADA. The site will serve as an informational network and advocacy tool of the ADA Watch coalition of disability rights organizations. Organizations include ADAPT, the American Association of People with Disabilities AAPD ; , the Bazelon Center for Mental Health Law, the Disability Rights Center, the National Association of Protection and Advocacy System, the National Council on Independent Living, the National Disabled Student Union, the National Organization on Disability and many others. Access the web site at adawatch, for instance, amiloride enac.
GLUCOCORTICOID REGULATION OF SODIUM TRANSPORT GENES REFERENCES 1. Alvarez de la Rosa D, Canessa CM, Fyfe GK, and Zhang P. Structure and regulation of amiloride-sensitive sodium channels. Annu Rev Physiol 62: 573594, 2000. de la Rosa D, Gimenez I, Forbush B, and Canessa CM. SGK1 activates Na -K -ATPase in amphibian renal epithelial cells. J Physiol Cell Physiol. First published September 28, 2005; doi: 10.1152 ajpcell.00556.2004. 2. Arystarkhova E and Wetzel RK. Gamma structural variants differentially regulate Na, K-ATPase properties. Ann NY Acad Sci 986: 416 419, Barquin N, Ciccolella DE, Ridge KM, and Sznajder JI. Dexamethasone upregulates the Na-K-ATPase in rat alveolar epithelial cells. J Physiol Lung Cell Mol Physiol 273: L825L830, 1997. 4. Bartholome B, Spies CM, Gaber T, Schuchmann S, Berki T, Kunkel D, Bienert M, Radbruch A, Burmester GR, Lauster R, Scheffold A, and Buttgereit F. Membrane glucocorticoid receptors mGCR ; are expressed in normal human peripheral blood mononuclear cells and upregulated after in vitro stimulation and in patients with rheumatoid arthritis. FASEB J 18: 70 80, Blum A and Maser E. Enzymology and molecular biology of glucocorticoid metabolism in humans. Prog Nucleic Acid Res Mol Biol 75: 173216, 2003. Chen SY, Bhargava A, Mastroberardino L, Meijer OC, Wang J, Buse P, Firestone GL, Verrey F, and Pearce D. Epithelial sodium channel regulated by aldosterone-induced protein sgk. Proc Natl Acad Sci USA 96: 2514 2519, Coetzee WA, Amarillo Y, Chiu J, Chow A, Lau D, McCormack T, Moreno H, Nadal MS, Ozaita A, Pountney D, Saganich M, VegaSaenz de Miera EC, and Rudy B. Molecular diversity of K channels. Ann NY Acad Sci 868: 233285, 1999. Dagenais A, Denis C, Vives MF, Girouard S, Masse C, Nguyen T, Yamagata T, Grygorczyk C, Kothary R, and Berthiaume Y. Modulation of -ENaC and 1-Na -K -ATPase by cAMP and dexamethasone in alveolar epithelial cells. J Physiol Lung Cell Mol Physiol 281: L217L230, 2001. 10. Debonneville C, Flores SY, Kamynina E, Plant PJ, Tauxe C, Thomas MA, Munster C, Chraibi A, Pratt JH, Horisberger JD, Pearce D, Loffing J, and Staub O. Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na channel cell surface expression. EMBO J 20: 70527059, 2001. Dong Y, Poellinger L, Gustafsson JA, and Okret S. Regulation of glucocorticoid receptor expression: evidence for transcriptional and posttranslational mechanisms. Mol Endocrinol 2: 1256 1264, Duc C, Farman N, Canessa CM, Bonvalet JP, and Rossier BC. Cell-specific expression of epithelial sodium channel alpha, beta, and gamma subunits in aldosterone-responsive epithelia from the rat: localization by in situ hybridization and immunocytochemistry. J Cell Biol 127: 19071921, 1994. Edwards CR, Stewart PM, Burt D, Brett L, McIntyre MA, Sutanto WS, de Kloet ER, and Monder C. Localisation of 11 beta-hydroxysteroid dehydrogenasetissue specific protector of the mineralocorticoid receptor. Lancet 2: 986 989, Friedrich B, Feng Y, Cohen P, Risler T, Vandewalle A, Broer S, Wang J, Pearce D, and Lang F. The serine threonine kinases SGK2 and SGK3 are potent stimulators of the epithelial Na channel alpha, beta, gammaENaC. Pflugers Arch 445: 693 696, Gallazzini M, Attmane-Elakeb A, Mount DB, Hebert SC, and Bichara M. Regulation by glucocorticoids and osmolality of expression of ROMK Kir 1.1 ; , the apical K channel of thick ascending limb. J Physiol Renal Physiol 284: F977F986, 2003. 16. Granitzer M, Mountian I, and Van Driessche W. Effect of dexamethasone on sodium channel block and densities in A6 cells. Pflugers Arch 430: 493500, 1995. Haarman EG, Kaspers GJ, Pieters R, Rottier MM, and Veerman AJ. Glucocorticoid receptor alpha, beta and gamma expression vs in vitro glucocorticod resistance in childhood leukemia. Leukemia 18: 530 537, Hao H, Wendt CH, Sandhu G, and Ingbar DH. Dexamethasone stimulates transcription of the Na -K -ATPase 1 gene in adult rat lung epithelial cells. J Physiol Lung Cell Mol Physiol 285: L593L601, 2003. physiolgenomics.
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Evaluating effectiveness The level of rigour of this evaluation should be similar to that used by competent drug regulatory agencies e.g. FDA, EMEA ; for the clinical evaluation of medicines submitted for marketing approval. Important considerations include the types of studies e.g. RCT, observational, or PK, PD the quality of the study independent of study type the validity and strength of evidence; and its applicability to the relevant paediatric population e.g. defined by different ages or disease states ; . Accepted guidelines for critical appraisal of therapeutic studies, for grading of "strength of evidence" and for deciding about applicability of research evidence to different patient circumstances can be used in answering this question. 41 ; 42 ; The randomised controlled clinical trial RCT ; is widely accepted as the gold standard study design for determining the effectiveness of interventions, with some exceptions. 43 ; While high quality RCTs remain the ideal, they do have a number of acknowledged limitations, especially those performed specifically for gaining marketing approval. 40 ; These include relatively small numbers of included subjects especially in published paediatric RCTs 44 and short duration of followup, both of which limit their usefulness in determining effectiveness and safety ; , especially in the treatment of chronic childhood conditions. In addition, subjects included in RCTs are often homogeneous and results may not be generalisable to the general paediatric population. A particular example of this is the issue of the different age groups that are encompassed by paediatrics neonates; infants; children; and adolescents ; . There are large variations in drug handling and response between these age groups and so studies conducted in the relevant age groups are needed to inform decisions about medicines intended for use in that age group. Systematic reviews of RCTs may be able to overcome some but not necessarily all of these limitations. A number of innovative trial designs have been developed to facilitate the study of small numbers of patients, which are particularly relevant for the study of uncommon or rare but serious childhood diseases. These include adaptive designs, such as Bayesian sequential studies; 45 ; randomized withdrawal designs; 46 ; the randomized placebo phase design; 47 ; and "n of 1" studies for populations. 48 ; Some of these study types may offer additional advantages over traditional RCTs, such as helping determine optimal patient and dose selection. Studies using such designs have been conducted in the paediatric population and should be sought to inform treatment decisions where available. While such studies are currently not numerous, it can be anticipated that their number is likely to increase in the future as more paediatric medicines research networks are established and become operational to address the increasing demand for better evidence about medicines for use in the paediatric population. Another important aspect of assessing effectiveness is whether outcomes that are clinically meaningful to the paediatric population have been evaluated in a particular study. 49 ; These may include patientbased outcomes such as symptom scores or quality of life measures validated in the relevant paediatric population ; or paediatric specific ones, such as developmental, learning and behavioural outcomes. In some cases, a well designed and conducted observational study e.g. prospective cohort study ; evaluating clinically meaningful outcomes at relevant time points may be preferable to a RCT that does not.
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In the postnatal lamb lung preparation, the pharmacology of inhibition of lung fluid reabsorption is consistent with the involvement of cyclic nucleotide-gated cation channels 27 ; , a notion supported recently by Norlin and colleagues 40 ; who have shown direct upregulation of amiloride-insensitive fluid reabsorption by cGMP; expression of this phenotype appears to be under developmental control since pimozide a cyclic nucleotide-gated cation channel blocker ; is ineffective in fetal lamb lung 26 ; . Recently, these in vivo data have been corroborated in a cellular system by demonstrating amiloride-insensitive, cGMP-evoked whole cell sodium currents in postnatal rat alveolar epithelial cells sensitive to blockade by pimozide and di trivalent cations, including Zn2 28 ; . Clearly, together, these recent findings suggest the scenario that such cyclic nucleotide-gated cation channels are an important contributor to adult lung fluid homeostasis perhaps both sodium absorption and potassium secretion ; . Intriguingly, the very recent data of Ehrhardt and colleagues 18 ; employing monolayers of human alveolar epithelial cells see below ; clearly show that, quantitatively, the most significant component of the shortcircuit current is Zn2 sensitive, suggesting that cyclic nucleotide-gated cation channels may be important in adult human alveolar epithelial ion and fluid handling. In addition to the essential role of amiloride-sensitive and -insensitive sodium channels, there is overwhelming evidence for the functional expression of a number of other ion conductances. These include calcium-sensitive and -insensitive potassium channels 15, 29, 32, ; , proton channels see below and Refs. 13 and 14 ; , and chloride channels, including cystic fibrosis transmembrane conductance regulator CFTR ; see below and Refs. 9, 24, 30, and 42 ; . Although the possible role of these ion channels in alveolar fluid homeostasis has been reviewed by various researchers 34, 42 ; , exact mechanistic information is still rather lacking. For example, active secretion of potassium has been alluded to in isolated perfused rat lung studies 5 ; , but currently we cannot be sure which specific channel types are involved. It is of interest, however, that Leroy and colleagues 32 ; have recently reported the presence of ATP-sensitive potassium channels in the alveolar epithelium which may, in combination with voltage-dependent and calcium-sensitive potassium channels, contribute to transepithelial transport of sodium and chloride by maintaining the electrochemical driving force across the alveolar epithelium. Of further importance to alveolar homeostasis may be to understand how these ion channels are regulated by neurohumoral factors under pathophysiological conditions [e.g., acute respiratory distress syndrome and congestive heart failure CHF ; ]. In this regard, some factor s ; in lung edema fluid have been reported to stimulate short-circuit current across rat distal lung epithelial cell monolayers 47 ; . Similarly, the stimulatory role of proteinase for sodium absorption across lung epithelial barrier s ; has been a focus of intense research 17, 51 ; . A particularly important area of interest in pathophysiology of the lung is CHF 46, 47, 49, ; , for which some exciting new!
Cozaar drug interactions tell your doctor of all nonprescription and prescription medication you are using, especially : if you are taking a potassium supplement such as k-dur, klor-con, and others, taking a potassium-sparing diuretic water pill ; such as amiloride midamor ; , spironolactone aldactone ; , or triamterene dyrenium, dyazide, maxzide ; , or using a salt substitute and elavil.
Fig. 5. Genistein activates Cl-selective potentials in CF patients with G551D mutation. A: measurement of nasal potential difference PD ; in a healthy subject. Negative intranasal potentials are plotted downward in all graphs. All drug treatments were additive. Note that perfusion with Cl-free solution, isoproterenol isoprot ; , and genistein resulted in significant hyperpolarizations, respectively. B: measurement of nasal PD in a G551D CF patient. Patient was a 14-year-old Caucasian female with genotype G551D F508. Note y-axis scaling. Perfusion with Cl-free solution consistently caused a depolarization likely caused by a tip potential at voltage-sensing electrode. Isoproterenol 10 M ; in Cl-free solution showed no effect, which is typical for recordings in CF patients 20 ; . Genistein 30 M ; significantly hyperpolarized nasal PD. C: average responses of G551D CF patients n 5 ; to treatment with amiloride amil, 50 M ; , Cl-free solution exchanged for gluconate ; and 10 M isoproterenol Cl free iso ; , and 30 M genistein geni ; , in comparison to measurements in healthy subjects n 8 ; . patients were 2 males and 3 females, ages 10, 14, 15, and 37. Genotypes and responses of PD to genistein ; of patients were: three G551D F508 0.8, 2.4, and 2.3 mV ; , one G551D G551D 2.0 mV ; , and one G551D unknown 4.3 mV ; . Responses of nasal PD to treatment with amiloride and Cl free iso were significantly different between CF and normal subjects P 0.01 ; , whereas response to treatment with genistein was not P 0.05, t-tests ; . Average nasal PD during initial NaCl perfusion was 16.1 1.4 mV in normals. In G551D CF patients average nasal PD values were: NaCl, 33.8 3.2 mV; amiloride, 11.7 0.9 mV; isoproterenol Cl free, 6.4 1.7 mV; and genistein, 8.7 1.6 mV. Readings were taken after 2 min after change of conditions when PD reached stable values and represent the numerical average of a 20-s period.
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Abramcheck, F. J., W. Van Driessche, and S. I. Helman. 1985. Autoregulation of apical membrane Na permeability of tight epithelia. Noise analysis with aniloride and CGS 4270. J. Gen. Physiol. 85: 555582. Atia, F., W. Zeiske, and W. Van Driessche. 1999. Secretory apical Cl channels in A6 cells: possible control by cell Ca2 and cAMP. Pflugers Arch. 438: 344 353. Awayda, M. S., W. Van Driessche, and S. I. Helman. 1999. Frequencydependent capacitance of the apical membrane of frog skin: dielectric relaxation processes. Biophys. J. 76: 219 232. Baxendale-Cox, L. M., R. L. Duncan, X. Liu, K. Baldwin, W. J. Els, and S. I. Helman. 1997. Steroid hormone-dependent expression of blockersensitive ENaCs in apical membranes of A6 epithelia. Am. J. Physiol. Cell Physiol. 273: C1650 C1656. Brazy, P. C., and R. B. Gunn. 1976. Furosemide inhibition of chloride transport in human red blood cells. J. Gen. Physiol. 68: 583599. Butterworth, M. B., S. I. Helman, and W. J. Els. 2001. cAMP-sensitive endocytic trafficking in A6 epithelia. Am. J. Physiol. Cell Physiol. 280: C752C762. Chalfant, M. L., B. Coupaye-Gerard, and T. R. Kleyman. 1993. Distinct regulation of Na reabsorption and Cl secretion by arginine vasopressin in the amphibian cell line A6. Am. J. Physiol. Cell Physiol. 264: C1480 C1488. Els, W. J., and S. I. Helman. 1981. Vasopressin, theophylline, PGE2, and indomethacin on active Na transport in frog skin: studies with microelectrodes. Am. J. Physiol. Renal Physiol. 241: F279 F288. Els, W. J., and S. I. Helman. 1997. Dual role of prostaglandins PGE2 ; in regulation of channel density and open probability of epithelial Na channels in frog skin R. pipiens ; . J. Membr. Biol. 155: 75 87. Fan, P. Y., M. Haas, and J. P. Middleton. 1992. Identification of a regulated Na K Cl cotransport system in a distal nephron cell line. Biochim. Biophys. Acta Bio-Membr. 1111: 75 80. Hall, W. J., J. P. O'Donoghue, M. G. O'Regan, and W. J. Penny. 1976. Endogenous prostaglandins, adenosine 3 : 5 -monophosphate and sodium transport across isolated frog skin. J. Physiol. Lond ; . 258: 731753. Helman, S. I., and L. M. Baxendale. 1990. Blocker-related changes of channel density. Analysis of a three-state model for apical Na channels of frog skin. J. Gen. Physiol. 95: 647 678. Helman, S. I., and X. Liu. 1997. Substrate-dependent expression of Na transport and shunt conductance in A6 epithelia. Am. J. Physiol. Cell Physiol. 273: C434 C441. Helman, S. I., X. Liu, K. Baldwin, B. L. Blazer-Yost, and W. J. Els. 1998. Time-dependent stimulation by aldosterone of blocker-sensitive ENaCs in A6 epithelia. Am. J. Physiol. Cell Physiol. 274: C947C957. Biophysical Journal 81 2 ; 852 866 and caduet.
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Candidates for subsequent in vivo testing in a Tg assay: whether drug solubility in acetone or ethanol was sufficient to elicit systemic toxicity; the level of gadd153, -globin, and c-fos promoter inductions by the drug; the potency of the drug in the in vitro assays; and the cost of the drug required for 6 months of dosing. Based on these criteria, amiloride, dipyridamole, and pyrimethamine were selected for testing the specificity of the Tg assay towards pharmacologically active, noncarcinogenic drugs and ascorbic!
Stop-flow studies in dogs indicate that amilride hydrochloride inhibits tubular secretion of potassium and reabsorption of sodium in the distal portion of the nephron. In renal clearance studies, 1.0 mg kg intravenously did not affect glomerular filtration rate, effective renal plasma flow, or glucose reabsorption. An enzymatic basis for the renal action of amiloride hydrochloride has not been elucidated. It is not an inhibitor of carbonic anhydrase.
Michael T Mann, Sharon Fowler, Kelly J Hunt, Roy Resendez, Ken Williams, Michael Stern; Univ of Texas Health Science Cntr at San Antonio, San Antonio, TX To address whether the inclusion of former drinkers as "non-drinkers" in cross-sectional studies artificially inflates the apparent protective effect of alcohol against cardiovascular mortality CVM ; , we used Cox proportional hazard models to compare mortality among four groups within the San Antonio Heart Study SAHS ; : drinkers, abstainers, quitters, and adopters , . -, and - , respectively, for reported alcohol use at the first and second exams ; . The SAHS, a population-based prospective cohort study, included 2754 participants aged 35 to 64 years at their first exam, who returned for a second exam 7.7 years later. Vital status ascertainment for this group was 99% as of the year 2000 7.9-year mean mortality follow-up and chlorthalidone.
In no case was there any pulmonary discomfort or noticeable effect on the central nervous system. Eye irritation, occurring immediately , was not more than slight until the level of 25 ppm was reached, although nose irritation was regarded as at least moderate by four of seven subjects at 12.5 ppm. Olfactory cognition was checked off as more than moderate only at 6.25 ppm, and by only two of five subjects. + ppm No. Eye Nose of subjects irritation irritation + A B 0.78 6 0 0 6.25 6 1 0 12.5 0 25.0 ppm No. Pulmonary Olfactory of subjects Discomfort Cognition + A B 0.78 6 0 0 6.25 0 0 12.5 0 0 25.0 0 0 ppm No. CNS of subjects Effects + A B 0.78 6 0 0 6.25 6 0 0 12.5 7 0 0 25.0 5 0 0 Note: Under A are listed the number showing any response at all; Under B, those listing higher responses than slight. 4 ; not assignable 39 ; Human - Medical Data The following medical procedures should be made available to each employee who is exposed 2-propen-1-ol at potentially hazardous levels: Initial Medical Screening: Employees should be screened for history of certain medical conditions which might place the employee at increased risk from 2-propen-1-ol exposure. Chronic respiratory disease: In persons with impaired pulmonary function, especially those with obstructive airway diseases, the breathing of 2-propen-1-ol might cause exacerbation of symptoms due to its irritant properties. Skin disease: 2-propen-1-ol can cause skin burns. Persons with existing skin disorders may be more susceptible to the effects of this agent. Liver disease: the UNEP PUBLICATIONS 221.
Behavioural Counselling interventions in Primary Care to reduce risky harmful alcohol use by adults: A summary of the evidence for the U.S. Preventive Services Task Force Annals of Internal Medicine 6 April 2004 Vol140 7 ; : 557-568 Link and tenoretic.
HENaC and PD. Since we examined only healthy adult males in this study, the range of values detected may be too narrow to adequately demonstrate a relationship between and hENaC mRNA expression and biologic activity. Future studies, described below, will reexamine these relationships as they relate to lung development, injury, and disease. The sensitivity of the QRTPCR assay will make it valuable in studying clinically relevant patient populations. Considerable evidence shows that removal of excess liquid from the air spaces of the lung is primarily driven by active Na transport across the tight alveolar epithelial barrier 38 ; . There is clinical evidence that patients with pulmonary edema who can reabsorb some alveolar edema fluid within 12 h after intubation and acute lung injury exhibit more rapid recovery from respiratory failure, and a lower mortality 18 ; . This was demonstrated by quantitation of the edema-fluid protein concentration in sequential samples of lung fluid from mechanically ventilated adult patients suffering from either high-pressure or high-permeability pulmonary edema. In addition, a recent study of preterm infants showed that the amiloride-sensitive nasal PD was significantly lower in infants in whom RDS subsequently developed, than in those who did not go on to develop RDS 14 ; . Application of QRTPCR in similar patient groups would allow us to elucidate the role of transcriptional regulation of hENaC in the resolution of pulmonary edema. Furthermore, the ability to measure hENaC mRNA levels may lead to an improved understanding of the genotypephenotype correlation in CF lung disease.
Later studies at the NIH established the exact site of action of the drug it inhibited the very last step on the synthetic pathway, i.e., the conversion of desmosterol to cholesterol 18 ; , by reduction of the side-chain double bond. Knowing the site of inhibition led to a number of findings that challenged the value of triparanol. For example, it was shown that large amounts of desmosterol accumulated in the plasma of treated animals and patients, accounting for up to 30% of total plasma sterols 19 ; . A key point of and atomoxetine and amiloride, for instance, amiloride spironolactone.
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Having structured knowledge in computable form will accelerate research in pharmacogenomics and other health disciplines. Using tools that can automatically extract the knowledge from unstructured literature will ensure access to the most current known information. Once these knowledge bases are available, researchers will be able to develop algorithms that can link diverse types of biological data to propose novel, and perhaps clever, biological hypotheses. Only at that point will the scientific community have met the challenge presented by Swanson, when he threw down the gauntlet and charged the community to find the "undiscovered public knowledge." 126 and strattera.
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Statements of Credit--Participants who successfully complete this activity including completion and submission of the evaluation form ; will be issued a statement of credit via e-mail or US mail within 4 weeks. Physicians. The Meniscus Educational Institute is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The Meniscus Educational Institute designates this educational activity for a maximum of 2 category 1 credits toward the AMA Physician's Recognition Award. Each physician should claim only those credits that he she actually spent in the educational activity. This activity has been reviewed and is acceptable for up to 2 prescribed credit hours by the American Academy of Family Physicians. Term of approval is for one year from beginning distribution date of November 20, 2002, with option to request yearly renewal. Nurses. This activity for 1.7 contact hours is provided by the Meniscus Educational Institute, which is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. Accreditation refers to recognition of educational activities only and does not imply approval or endorsement of any product by the American Nurses Credentialing Center's Commission on Accreditation. Provider approved by the California Board of Registered Nursing, Provider No. 13164, for 1.7 contact hours. Pharmacists. This educational activity is sponsored by the Meniscus Educational Institute. The Meniscus Educational Institute is accredited by the American Council on Pharmaceutical Education ACPE ; as a provider of continuing pharmaceutical education. The ACPE Universal Program Number assigned to this program, for 1.5 contact hours 0.15 CEU ; , is 429-000-02-014-H01. Physician Assistants. This program has been reviewed and is approved for a maximum of 2 hours of clinical Category I Preapproved ; CME credit by the American Academy of Physician Assistants. Approval is valid for 2 years from the issue date of November 2002. Participants may submit the self-assessment at any time during that period. This program has been planned in accordance with AAPA's CME Standards for Enduring Materials Programs and for Commercial Support of Enduring Material Programs. Respiratory Therapists. This educational activity has been granted Category I approval by the American Association for Respiratory Care for 2 hours of CRCE credit.
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Adapted from forecast disclosed on Form 8-K, filed on February 10, 2006. a ; Forecasts in the table exclude the effects of business-development transactions not completed as of December 31, 2005. Forecasts in the table do not include the potential impact from a substantial prospective gain on the divestiture of our Consumer Healthcare business, as well as costs related to our recently announced sales-force restructuring. b ; Primarily reflects the reclassification of our Consumer Healthcare business to discontinued operations and amiodarone.
The health hazards of exposure to lead are well known. In recent years, much attention has been paid to the fact that calcium carbonate supplements contain trace amounts of lead. In one recent study, 4 of the 7 popular over-the-counter calcium carbonate supplements tested contained lead ~1mg day for 800 mg day of calcium and 1-2 mg day for 1500 mg day of calcium ; . 1 Whether or not such levels of exposure are a threat to health is an open question. Calcium is known to offset the effects of lead by blocking its absorption both in the supplement and in other dietary contributors of lead ; .2 In fact, research has shown that blood lead levels are lower in people who take calcium supplements than in those who do not.3 As a consequence, Robert P. Heaney, MD, of Creighton University, a leader in the field of calcium and bone, has written, "the calcium sources available today are generally very safe."2 In short, patients are safe taking calcium supplements from respected manufacturers. Patients should, however, avoid supplements derived from dolomite, bone meal, or unrefined oyster shell. Alternatives to calcium carbonate include calcium citrate, calcium phosphate, and by prescription ; calcium acetate. Be advised that calcium carbonate preparations are currently the least expensive and the most widely available.
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