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Indomethacin What form s ; does ratio-indomethacin come in. ACETAMINOPHEN W CODEINE ACYCLOVIR ALBUTEROL ALLOPURINOL ALPRAZOLAM AMITRIPTYLINE AMOXICILLIN AMPHETAMINE ATENOLOL BENZONATATE BUTALBITAL APAP CAFFEINE CAPTOPRIL CARBIDOPA LEVODOPA CARISOPRODOL CARTIA XT CEPHALEXIN CIMETIDINE, prescription strength CLINDAMYCIN CLONAZEPAM CLONIDINE CYCLOBENZAPRINE DEXAMETHASONE DIAZEPAM DICLOFENAC DICYCLOMINE DILTIA XT DILTIAZEM DOXAZOSIN DOXEPIN DOXYCYCLINE ESTRADIOL ESTROPIPATE FENOPROFEN FLUOXETINE FLURBIPROFEN FOLIC ACID, 1 mg. FUROSEMIDE GEMFIBROZIL GLIPIZIDE GLYBURIDE GLYBURIDE MICRONIZED HYDROCHLOROTHIAZIDE HYDROCODONE W ACETAMINOPHEN HYDROXYZINE HYOSCYAMINE IBUPROFEN, prescription strength IMIPRAMINE INDAPAMIDE INDOMETHACIN ISOSORBIDE DINITRATE ISOSORBIDE MONONITRATE LEVOTHROID LEVOXYL LISINOPRIL LORAZEPAM MEDROXYPROGESTERONE METFORMIN METHYLPHENIDATE METHYLPREDNISOLONE METOCLOPRAMIDE METOPROLOL METRONIDAZOLE, 250, 500 mg. MINOCYCLINE MIRTAZAPINE NAPROXEN. prescription strength NECON NEOMYCIN POLYMYXIN HC NIFEDIPINE, immediate release NITROGLYCERIN NORTRIPTYLINE NYSTATIN OXYBUTYNIN, immediate release OXYCODONE W ACETAMINOPHEN PENICILLIN PENTOXIFYLLINE POTASSIUM CHLORIDE PREDNISOLONE PREDNISONE PROMETHAZINE PROMETHAZINE W CODEINE PROPOXYPHENE W APAP PROPRANOLOL RANITIDINE SPIRONOLACTONE SULFAMETHOXAZOLE TRIMETHOPRIM SULFASALAZINE SULINDAC TAMOXIFEN TEMAZEPAM THEOPHYLLINE. The 21st annual meeting of the glomerular disease collaborative network gdcn ; april 29 april 30, 2006 the grove park inn, asheville, nc sponsored by the school of medicine of the university of north carolina at chapel hill. Stannous Fluoride Stannous Fluoride dental gel Stannous Fluoride dental rinse Star, The Jordan ; State Legislatures STATISTICA NEERLANDICA Statistical Journal of the UN Economic Commission for Europe Statistical Methods & Applications STATISTICAL METHODS IN MEDICAL RESEARCH Statistical Modelling: An International Journal STATISTICAL PAPERS STATISTICIAN Statistics and Probability Letters STATISTICS. STEEL TIMES INTERNATIONAL Stereo Review Steroids STOCHASTIC ANALYSIS AND APPLICATIONS Stochastic Environmental Research and Risk Assessment SERRA ; STOCHASTIC MODELS STOCHASTIC PROCESSES AND THEIR APPLICATIONS Stochastics : an international journal of probability and stochastic processes Stock Picks Bob's Advice Stores Magazine STRABISMUS. STRAD, for example, indomethacin headaches. Indomethacin ibuprofen interactionIndomethacin uv spectrumStakeholders suggested various negative consequences that might follow if the Australian Government did not continue to support the HMR. These included poorer health among older people and the chronically ill in particular, increased hospitalisation, reduced capacity for older people to remain in their own homes, and poorer patient quality of life. Such trends, a number of stakeholders believed, were likely to mean increased health costs both for the Australian Government eg through the PBS ; and for State and Territory Governments eg in hospital costs and imdur. The special syn-flex formula combines the latest scientific breakthroughs in the arthritis medical community into one product that is guaranteed to end your pain and halt your osteoarthritis. Monkey was randomly assigned to 1 of groups: 1 ; a spontaneous recovery group SR 2 ; a motor skill training group that received a single dose of saline on the 1st day of training Sal Training and 3 ; a motor skill training group that received a single dose of d-AMPH 0.25 mg kg i.m. ; on the first day of training d-AMPH Training ; . In a previous study, the 0.25 mg kg dose salt weight ; was determined to be an adequate psychoactive dose that did not interfere with squirrel monkeys' performance on a hand dexterity task.12 Saline or d-AMPH in an injection volume of 0.25 ml was given 1 h before training began. First, each monkey was adapted to a reach and retrieval task requiring the skilled use of digits, wrist, and forearm. The task required monkeys to retrieve small, banana-flavored food pellets 45 mg; BioServe, Frenchtown, NJ ; from food wells drilled into a Plexiglas board attached to each monkey's home cage modified Klver board ; . Each of the 5 food wells was 5 mm deep but differed in diameter well 1 25 mm, well 2 19.5 mm, well 3 13.5 mm, well 4 11.5 mm, and well 5 9.5 mm ; . Once a monkey could successfully retrieve food pellets from the Klver board flexions retrieval ; , hand preference and baseline values were established, pooled over the 5 food wells.13 Group values are henceforth presented as Mean SEM ; . Prior to the infarct, a 1-way ANOVA demonstrated that there were no statistically significant differences in flexions retrieval between monkeys in the SR group 2.57 0.4 flexions retrieval ; , Sal Training group 1.9 0.13 flexions retrieval ; , and d-AMPH Training group 2.33 0.18 flexions retrieval ; : F 2, 9 ; 1.76, P 0.23. An index of performance as described in a previous study14 was employed for further analysis to normalize each monkey's performance to his baseline flexions retrieval postinfarct score divided by baseline score ; . The index measures the degree of deviation from preinfarct performance. This normalization is needed to control within-group variance due to inherent individual variation in motor skills typically observed between squirrel monkeys on the Klver board task during baseline testing. Controlling for individual variation is especially important with the small sample sizes necessary in nonhuman primate studies. An index of 1 is equivalent to baseline performance, index scores below 1 are reflective of improvements from baseline performance, and index scores above 1 indicate a behavioral impairment relative to baseline values. Within days of establishing baseline values, the primary motor cortex M1 ; hand and bordering areas e.g., shoulder and face ; contralateral to each monkey's preferred hand were identified by intracortical microstimulation, ensuring that each monkey would receive a complete infarct to the distal hand area in the M1. Then an ischemic infarct was made by cauterizing surface 456 and sorbitrate. 1992; 121 5 Pt 1 ; 771-5. 35. Lam BC, Wong HN, Yeung CY. Effect of indomethacin on binding of bilirubin to albumin. Arch Dis Child 1990; 65: 690-1. Herson VC, Krause PJ, Eisenfeld LI, Pontius L, Maderazo EG. Indomethacin-associated sepsis in very-low-birth-weight infants. J Dis Child 1988; 142: 555-8. Meyers RL, Alpan G, Lin E, Clyman RI. Patent ductus arteriosus, indomethacin, and intestinal distension: effects on intestinal blood flow and oxygen consumption. Pediatr Res 1991; 29: 569-74. Coombs RC, Morgan ME, Durbin GM, Booth IW, McNeish AS. Gut blood flow velocities in the newborn: effects of patent ductus arteriosus and parenteral indomethacin. Arch Dis Child 1990; 65 10 Spec No ; : 1067-71. 39. Fujii AM, Brown E, Mirochnick M, O'Brien S, Kaufman G. Neonatal necrotizing enterocolitis with intestinal perforation in extremely premature infants receiving early indomethacin treatment for patent ductus arteriosus. J Perinatol 2002; 22: 535-40. Dumas de la Roque E, Fayon M, Babre F, Demarquez JL, Pedespan L. Minimal effective dose of indomethacin for the treatment of patent ductus arteriosus in preterm infants. Biol Neonate 2002; 81: 91-4. Nakamura T, Tamura M, Kadowaki S, Sasano T. Low-dose continuous indomethacin in early days of age reduce the incidence of symptomatic patent ductus arteriosus without adverse effects. J Perinatol 2000; 17: 271-5. Evans N, Iyer P. Change in blood pressure after treatment of patent ductus arteriosus with indomethacin. Arch Dis Child 1993; 68 5 Spec No ; : 584-7. 43. Mardoum R, Bejar R, Merritt TA, Berry C. Controlled study of the effects of indomethacin on cerebral blood flow velocities in newborn infants. J Pediatr 1991; 118: 112-5. Colditz P, Murphy D, Rolfe P, Wilkinson AR. Effect of infusion rate of indomethacin on cerebrovascular response in preterm neonates. Arch Dis Child 1989; 64 1 Spec No ; : 8-12. 45. Hammerman C, Glaser J, Schimmel MS, Ferber B, Kaplan M, Eidelman AI. Continuous versus multiple rapid infusions of indomethacin: effects on cerebral blood flow velocity. Pediatrics 1995; 95: 244-8. Van Bel F, Bartelds B, Teitel DF, Rudolph AM. Effect of indomethacin on cerebral blood flow and oxygenation in the normal and ventilated fetal lamb. Pediatr Res 1995; 38: 243-50. Schmidt B, Davis P, Moddemann D, et al. Long-term effects of indomethacin prophylaxis in extremely-low-birth-weight infants. N Engl J Med 2001; 344: 1966-72. Szymonowicz W, Yu VY. Periventricular haemorrhage: association with patent ductus arteriosus and its treatment with indomethacin or surgery. Aust Paediatr J 1986; 23: 21-5. Soll RF. Prophylactic natural surfactant extract for preventing morbidity and mortality in preterm infants. Cochrane Database Syst Rev 2000; CD000511. 50. Soll RF. Prophylactic synthetic surfactant for preventing morbidity and mortality in preterm infants. Cochrane Database Syst Rev 2000; CD001079. 51. Couser RJ, Ferrara TB, Wright GB, et al. Prophylactic indomethacin therapy in the first twenty-four hours of life for the prevention of patent ductus arteriosus in preterm infants treated prophylactically with surfactant in the delivery room. J Pediatr 1996; 128 5 Pt 1 ; 631-7. TABLE 174 Fluoride in the treatment of steroid-induced osteoporosis: details of included studies potential prognostic factors cont'd ; Mean BMD at lumbar spine g cm2 ; Subjects with Sex and menopausal status: vertebral fracture no. % ; at baseline: no. % ; No data No data Men Women 4 27 ; 11 Crohn's disease Men Women 10 56 ; 8 Crohn's disease 15 100 ; 11 100 ; 0.88 0.03 0.90 Underlying illness: no and imipramine. There's also a blackout period that lasts between four and eight hours, and, not surprisingly, these drugs can be fatal, because indomethacin suppository! Tors were detected in smooth muscle, but not in the endothelium, of abdominal aortas from WT or eNOS mice. However, the expression of ETA receptors was surprisingly decreased in aortas from eNOS mice. An explanation for this could be that the loss of NO may facilitate endothelial ET production, resulting in an increase in tissue or circulating ETs, which could then cause downregulation of smooth muscle ETA receptors.14, 15, 17, 22 Indeed, vessels from deoxycorticosterone acetate salt hypertensive rats which exhibit decreased endothelial NO activity ; were reported to have elevated local or circulating ET level and decreased expression of ETA receptors.2326 However, ETA receptor expression is also decreased in aortas from the spontaneously hypertensive rats, which appear to have normal vascular ET-1 content.22, 23, 27 Moreover, in eNOS mice, ET immunoreactivity in plasma was reported to be similar to that of control mice.18 Therefore, downregulation of ETA receptors could also be mediated by mechanisms that are independent of increased local or circulating ET levels. Regardless of the underlying mechanism, decreased expression of ETA receptors in eNOS mice would be expected to result in decreased rather than increased contraction to ETA receptor stimulation. In aortas from WT mice, the COX inhibitor indomethacin or TXA2 PGH2 receptor antagonist SQ-29548 inhibited contractions to ET-1 1-31 ; but did not affect responses to phenylephrine. These results suggested that contractions to ETA receptor activation are distinct from those induced by 1-adrenergic activation in being mediated by COX-derived metabolites. In a similar manner to ET-11 1-31 ; , the COX substrate arachidonic acid caused indomethacin-sensitive contractions of endothelium-denuded aortas that were significantly increased in blood vessels from eNOS compared with WT mice. Therefore, we considered that increased COX activity might be responsible for the enhanced contraction to ETA receptor stimulation in eNOS mice. This was confirmed by observations that ET-1 1-31 ; caused increased production of the TXA2 metabolite TXB2 in endotheliumdenuded abdominal aorta of eNOS mice compared with WT mice and that indomethacin prevented the increased contraction of eNOS aortas to ET-1 1-31 ; . In fact, after indomethacin, contractions to ETA receptor activation by ET-1 1-31 ; were decreased in aortas from eNOS compared with WT mice. These results indicate that increased activity of COX in eNOS aortas enables ETA receptor stimulation to overcome the decreased expression of the receptor, which would otherwise result in decreased contractility. Two isoforms of COX, COX-1 and COX-2, have been identified in cultured vascular smooth muscle cells.28, 29 In eNOS mice, the selective COX-2 inhibitor celecoxib or TXA2 PGH2 receptor antagonist SQ-29548 inhibited the contraction induced by ET-1 1-31 ; to a similar extent as the nonselective COX inhibitor indomethacin. This suggests that enhanced contraction to ET-1 1-31 ; in eNOS mice is mediated through the COX-2 isoform. Indeed, endotheliumdenuded abdominal aortas from WT and eNOS mice were found not to express COX-1, whereas COX-2 was found to be present in the medial layer of both blood vessels, with increased expression in aortas of eNOS compared with WT mice. Therefore, these results identify an important role and tofranil. Cc vn Tm Phn ln cc bnh nhn phn nn ko di kiu trm cm v lo nhiu mt bnh tt, nm vin, v tc ng trn nhn cch v gia nh Maunder ; . Cc bnh nhn khc thng bo mt ng mng. Khng nn coi nh cc kha cnh tm l x lin quan n bnh l ny v nghin cu su hn. Bn cnh nhng nh hng i vi bnh nhn, tc ng tm l trn nhn vin y t v gia nh h cng c ghi nhn l ng k Avendano ; . Ti liu tham kho 1. Avendano M, Derkach P, Swan S. Clinical course and management of SARS in health care workers in Toronto: a case series. CMAJ 2003; 168. Published online on June 24, 2003. : cmaj cgi content full 168 13 1649 Booth CM, Matukas LM, Tomlinson GA, et al. Clinical features and short-term outcomes of 144 patients with SARS in the greater Toronto area. JAMA 2003; 289: 2801-9. : SARSReference lit ?id 12734147 3. CDC. Preliminary Clinical Description of Severe Acute Respiratory Syndrome. MMWR 2003; 52: 255-6. : cdc.gov mmwr preview mmwrhtml mm5212a5 4. CDC. Severe Acute Respiratory Syndrome - Singapore, 2003. MMWR 2003; 52: 405-11. : cdc.gov mmwr preview mmwrhtml mm5218a1 5. CDC. Cluster of severe acute respiratory syndrome cases among protected health care workers Toronto, April 2003. MMWR 2003; 52: 433-6, for example, indomethacin suppository. The symbols and codes are explained at the bottom of each timetable page. Mae'r symbolau a'r codau wedi eu hegluro ar waelod pob tudalen amserlen and indapamide. Recently, BADGE, a synthetic compound that is used in the production of industrial plastics, was identified as a pure antagonist for the nuclear hormone receptor PPAR-, with micromolar affinity [7]. In this study, BADGE antagonized the ability of PPAR- agonists to activate the transcriptional and adipogenic effects of PPAR-. BADGE also blocked the ability of adipogenic cell lines to undergo hormone-mediated cell differentiation. In contrast, another report showed that BADGE acts as a PPAR agonist in an immortalized human umbilical vein endothelial cell line ECV304 ; [8]. In this cell line BADGE induced PPAR activation and nuclear localization of the receptor and initiated cell death. Previously, we found that PPAR- agonists cause apoptosis in colon carcinoma cell lines and are able to sensitize tumour cells against other proapoptotic stimuli [6]. As a putative PPAR- agonist, BADGE should exert similar effects on colon carcinoma cells. To test this hypothesis, we treated HCT-116 cells with BADGE in the absence and presence of indomethacin, which is known to be cytotoxic for colon cancer cells. BADGE potently induced apoptosis in HCT-116 cells in a concentrationdependent manner. Furthermore, BADGE sensitized these cells against indomethacin-induced apoptosis. Whereas regulation of lipid metabolism and adipocyte differentiation by PPAR- agonists are most probably mediated via PPAR-, PPAR- expression is not essential for PPAR- ligands to exert anti-inflammatory effects in macrophages [12] and antiproliferative effects in mouse embryonic stem cells [13]. To investigate whether PPAR- expression is required for the proapoptotic and sensitizing effect of BADGE, we incubated PPAR--negative Jurkat cells with a range of BADGE concentrations in the absence and presence of indomethacin. Surprisingly, as observed in experiments with HCT-116 cells, BADGE strongly induced cell death in Jurkat cells and sensitized these cells against indomethacin-caused apoptosis. This suggests that BADGE is able to induce cell death independently from PPAR- expression. Previously, we reported that the PPAR- agonist pioglitazone increases basal apoptosis cells and promotes TRAIL-induced cytotoxicity in Jurkat cells [6]. Since T-cells have been reported to express PPAR- we, unfortunately, did not test whether the Jurkat cells used for our experiments also expressed this tran. 4.2.3 Pharmacological management in adults and lozol. Spinal bone mineral content Postmenopausal women with 65.9 established osteoporosis at least one and maximum of three vertebral compression fractures sustained during minor trauma. Drug resistance is a serious issue in treating mac, but potent treatments can slow the development of drug-resistant mac bacteria and isoflavone and indomethacin, for instance, indomethacin patent. Activating subscriptions document delivery linking to ingentaconnect alerting & rss feeds other library services keeping in touch register indomethacin use for the management of patent ductus arteriosus in preterms: a web-based survey of practice attitudes among neonatal fellowship program directors in the united states authors: amin, 1 ; handley, c.
Drug indomethacin the suspension has been made to that uses outside of the honcode principles.
I would almost nothing works for me, ibuprofen doesn't do anything, indomethacin doesn't do anything, its horrible.
Or 100 IM in RPMI medium 1640 containing 10% FBS without phenol red, and indomethacin at 0.1, or 10 iM in the medium with phenol red and 10% FBS. Cell culture. On the basis of our having previously demonstrated that auricular skin inflammation was induced by quinolone phototoxicity in Balb c mice Shimoda et al., 1993 ; , Balb c 3T3 mouse fibroblast cells obtained from American Type Culture Collection and maintained in our laboratory were used in the present study. The cells were seeded in 12well culture plates coated with collagen type I Iwaki Glass, Japan ; at a uniform density of 5 X 104 cells ml in RPMI medium 1640 with phenol red, supplemented with 10% FBS, penicillin 100 zg ml ; , and streptomycin 100 units ml ; , followed by incubation for 72 hr at 37C in a humidified 5% CO 2 incubator to approximately 100% monolayer confluence. Prior to use in the experiments, the cells were rinsed once with RPMI medium 1640 without phenol red. UVA source and irradiation. Three FL20SBLB black light tubes Toshiba Co. Ltd., Japan ; , emitting radiation from 300 to 400 nm, were used as UVA source. Immediately after the test compound solution was added to the well, the culture plates were covered with a 3-mm-thick pane of glass to eliminate wavelengths below 320 nm and irradiated with UVA at 1.5 mW cm2 for 5 min 0.5 J cm 2 ; UVA intensity was measured at 365 nm using a UVX digital radiometer fitted with a UVX-36 sensor UVP Inc., U.S.A. ; . This UVA dose was confirmed in a preliminary study not to induce the elevation of PGE? concentration in the incubation medium or morphological changes in 3T3 cells. Effects of simultaneous treatment with quinolone and UVA on the release of PCE2, 6-keto-PGF' LTB4 and lactate dehydrogenase LDH ; from 3T3 cells. After 1 ml of phenol red-free RPMI medium containing SPFX or LVFX at 1, 10, or 100 IM was added to the well, the culture plates were irradiated with UVA for 5 min. For the vehicle control, quinolone-free medium without phenol red was added to the well. For the non-UVA control, the culture plates were kept for 5 min under the ambient conditions of an experimental room in which UVA intensity was detected at less than 0.01 mW cm2. The quinolone solution was then replaced with the medium containing 10% FBS, and the culture plates were placed in the incubator for 24 hr. The incubation medium was then collected and centrifuged at 800 rpm for 5 min, and the supernatant was stored at -20C until use for eicosanoid or LDH assay. PGE 2 concentration was measured for all samples, but those of 6-keto-PGF lo , LTB 4 , and LDH were measured only in the samples of the vehicle control, 100 JXM SPFX, and 100 IM LVFX groups. I$ffect of UVA-preirradiated quinolone on PGE2 production. SPFX and LVFX solutions were irradiated with UVA for 5 min in advance and then applied to the cells. The plates were placed under the ambient room conditions for 5 min. For the vehicle control, the cells were incubated in RPMI medium 1640 preirradiated with UVA for 5 min. These culture media.
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FIG. 1. Suppression of aromatase activity in SK-BR-3 breast cancer cells by NSAIDs and COX-1 selective inhibitor. SK-BR-3 cells were treated with indomethacin E ; , piroxicam F ; , ibuprofen f ; , or SC560 ; , and aromatase activity was measured as described in Materials and Methods. Values are expressed as picomoles 3H2O formed per hour incubation time per million live cells. The results were normalized against a control treatment with vehicle. The value of 100% is equal to 0.003 pmol h 106 cells. Each data point represents the mean results of three independent determinations.
Keirse MJ. New perspectives for the effective treatment of preterm labor. American Journal of Obstetrics & Gynecology 1995; 173: 618-28. Lockwood CJ, Wein R, Lapinski R, Casal D, Berkowitz G, Alvarez M, Berkowitz RL. The presence of cervical and vaginal fetal fibronectin predicts preterm delivery in an inner-city obstetric population. American Journal of Obstetrics & Gynecology 1993; 169: 798-804. British Medical Association; Royal Pharmaceutical Society of Great Britain. British National Formulary March 1993 ; . Bath: The Bath Press; 1993. Ballard P, Ballard R. Scientific basis and therapeutic regimens for use of antenatal glucocorticoids. J Obstet Gynecol 1995; 173: 254-62. Howie R, Liggins G. Farrell P, editors.Lung development: biological and clinical perspectives. New York: Academic Press; 1982; The New Zealand study of antepartum glucocorticoid treatment. p. 255-65. Canadian Preterm Labor Investigators Group. Treatment of preterm labor with the B-adrenergic agonist ritodrine. New Engl J Med 1992; 327: 308-12. Keirse MJNC. Betamimetic tocolytics in preterm labour [revised 17 February 1993]. In: Keirse MJNC, Renfrew MJ, Neilson JP, Crowther C eds ; Pregnancy and Childbirth Module. In: The Cochrane Collaboration; Issue 2, Oxford: Update Software; 1995. Available from BMJ Publishing Group, London Higby K, Xenakis EM, Pauerstein CJ. Do tocolytic agents stop preterm labor? A critical and comprehensive review of efficacy and safety. American Journal of Obstetrics & Gynecology 1993; 168: 1247-56; disc. Lamont RF. The contemporary use of B agonists. Br J Obstet Gynaecol 1993; 100: 890-2. Scientific Advisory Committee of RCOG. RCOG Guidelines No.1 For the use of ritodrine. Keirse MJNC. Indomethaciin tocolysis in preterm labour [revised 14 August 1992]. In: Keirse MJNC, Renfrew MJ, Neilson JP, Crowther C eds ; Pregnancy and Childbirth Module, In: The Cochrane Collaboration; Issue 2, Oxford: Update Software; 1995. Available from BMJ Publishing Group, London. Bivins HA, Jr., Newman RB, Fyfe DA, Campbell BA, Stramm SL. Randomized trial of oral indomethacin and terbutaline sulfate for the long-term suppression of preterm labor. American Journal of Obstetrics & Gynecology 1993; 169: 1065-70. Saenger JS, Mayer DC, D'Angelo LJ, Manci EA. Ductus-dependent fetal cardiac defects contraindicate indomethacin tocolysis. Journal of Perinatology 1992; 12 1 ; : 41-7. Eronen M, Pesonen E, Kurki T, Teramo K, Ylikorkala O, and Hallman M. Increased incidence of bronchopulmonary dysplasia after antenatal administration of indomethacin to prevent preterm labor. Journal of Pediatrics 1994; 124 5 Pt 1 782-8. Major C, Lewis D, Harding J, Porto M, and Garite T. Tocolysis with indomethacin increases the incidence of necrotizing enterocolitis in the low-birth-weight neonate. American Journal of Obstetrics & Gynecology 1994; 170 1 Pt 1 102-6. Gloor J, Muchant D, and Norling L. Prenatal maternal indomethacin use resulting in prolonged neonatal renal insufficiency . Journal of Perinatology 1993; 13 6 ; : 425-7. Walker MP, Cantrell CJ. Maternal renal impairment after indomethacin tocolysis. Journal of Perinatology 1993; 13 6 ; : 461-3. Kupferminc M, Lessing JB, Yaron Y, Peyser MR. Nifedipine versus ritodrine for suppression of preterm labour. British Journal of Obstetrics & Gynaecology 1993; 100: 1090-4. Crowther C, Alfirevic Z. Keirse MJNC, Renfrew MJ, Neilson JP, Crowther C, editors.Pregnancy and Childbirth Module. In: The Cochrane Database of Systematic Reviews [database on disk and CDROM].
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