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Deslanoside, Cont. ; 1 Chlorthalidone, 446 1 Cyclothiazide, 446 2 Dextrothyroxine, 448 1 Ethacrynic Acid, 442 1 Furosemide, 442 4 Gallamine Triethiodide, 443 4 Glyburide, 445 1 Hydrochlorothiazide, 446 1 Hydroflumethiazide, 446 1 Indapamide, 446 2 Levothyroxine, 448 2 Liothyronine, 448 2 Liotrix, 448 1 Loop Diuretics, 442 2 Methimazole, 447 1 Methyclothiazide, 446 1 Metolazone, 446 4 Nondepolarizing Muscle Relaxants, 443 4 Pancuronium, 443 1 Polythiazide, 446 2 Propylthiouracil, 447 1 Quinethazone, 446 4 Succinylcholine, 444 4 Sulfonylureas, 445 1 Thiazide Diuretics, 446 2 Thioamines, 447 2 Thyroglobulin, 448 2 Thyroid, 448 2 Thyroid Hormones, 448 4 Tolbutamide, 445 1 Trichlormethiazide, 446 Desogen, see Contraceptives, Oral Desoxycorticosterone, 1 Ambenonium, 61 1 Anticholinesterases, 61 2 Aspirin, 1042 2 Bismuth Subsalicylate, 1042 2 Choline Salicylate, 1042 1 Edrophonium, 61 5 Isoniazid, 714 2 Magnesium Salicylate, 1042 1 Neostigmine, 61 1 Pyridostigmine, 61 2 Salicylates, 1042 2 Salsalate, 1042 2 Sodium Salicylate, 1042 2 Sodium Thiosalicylate, 1042 Desoxyn, see Methamphetamine Desyrel, see Trazodone Devrom, see Bismuth Subgallate Dexamethasone, 5 Aluminum Hydroxide, 367 5 Aluminum-Magnesium Hydroxide, 367 1 Ambenonium, 61 2 Aminoglutethimide, 366 2 Amobarbital, 369 4 Anisindione, 82 5 Antacids, 367 1 Anticholinesterases, 61 4 Anticoagulants, 82 2 Aprobarbital, 369 2 Aspirin, 1042 2 Barbiturates, 369 2 Bismuth Subsalicylate, 1042 2 Butabarbital, 369 2 Butalbital, 369 2 Choline Salicylate, 1042 4 Dicumarol, 82 1 Edrophonium, 61 5 Ephedrine, 372 2 Ethotoin, 374 Dexamethasone, Cont. ; 2 Fosphenytoin, 374 2 Hydantoins, 374 5 Interferon Alfa, 706 5 Isoniazid, 714 5 Magnesium Hydroxide, 367 2 Magnesium Salicylate, 1042 2 Mephenytoin, 374 2 Mephobarbital, 369 1 Neostigmine, 61 4 Nondepolarizing Muscle Relaxants, 894 4 Pancuronium, 894 2 Pentobarbital, 369 2 Phenobarbital, 369 2 Phenytoin, 374 2 Primidone, 369 1 Pyridostigmine, 61 1 Rifabutin, 376 1 Rifampin, 376 1 Rifamycins, 376 1 Rifapentine, 376 2 Salicylates, 1042 2 Salsalate, 1042 2 Secobarbital, 369 2 Sodium Salicylate, 1042 2 Sodium Thiosalicylate, 1042 4 Tubocurarine, 894 4 Vecuronium, 894 4 Warfarin, 82 Dexatrim, see Phenylpropanolamine Dexedrine, see Dextroamphetamine Dexfenfluramine, 4 Acetophenazine, 56 4 Chlorpromazine, 56 1 Fluoxetine, 1142 4 Fluphenazine, 56 1 Fluvoxamine, 1142 1 MAO Inhibitors, 55 4 Mesoridazine, 56 1 Paroxetine, 1142 4 Perphenazine, 56 1 Phenelzine, 55 4 Prochlorperazine, 56 4 Promazine, 56 1 Serotonin Reuptake Inhibitors, 1142 1 Sertraline, 1142 4 Thioridazine, 56 1 Tranylcypromine, 55 4 Trifluoperazine, 56 4 Triflupromazine, 56 Dextroamphetamine, 4 Acetophenazine, 56 3 Ammonium Chloride, 57 4 Chlorpromazine, 56 1 Fluoxetine, 1142 4 Fluphenazine, 56 1 Fluvoxamine, 1142 2 Furazolidone, 54 2 Guanethidine, 598 1 MAO Inhibitors, 55 4 Mesoridazine, 56 1 Paroxetine, 1142 4 Perphenazine, 56 1 Phenelzine, 55 4 Phenothiazines, 56 3 Potassium Acid Phosphate, 57 2 Potassium Citrate, 58 4 Prochlorperazine, 56 4 Promazine, 56 1 Serotonin Reuptake Inhibitors, 1142 1 Sertraline, 1142 Dextroamphetamine, Cont. ; 2 Sodium Acetate, 58 3 Sodium Acid Phosphate, 57 2 Sodium Bicarbonate, 58 2 Sodium Citrate, 58 2 Sodium Lactate, 58 4 Thioridazine, 56 1 Tranylcypromine, 55 4 Trifluoperazine, 56 4 Triflupromazine, 56 2 Tromethamine, 58 3 Urinary Acidifiers, 57 2 Urinary Alkalinizers, 58 Dextromethorphan, 4 Fluoxetine, 586 4 MAO Inhibitors, 431 4 Phenelzine, 431 3 Quinidine, 432 1 Sibutramine, 1062 3 Terbinafine, 433 4 Tranylcypromine, 431 Dextrothyroxine, 2 Aminophylline, 1220 5 Amitriptyline, 1278 5 Amoxapine, 1278 1 Anisindione, 85 1 Anticoagulants, 85 4 Beta Blockers, 249 2 Cholestyramine, 1233 5 Clomipramine, 1278 5 Desipramine, 1278 2 Deslanoside, 448 1 Dicumarol, 85 2 Digitalis, 448 2 Digitalis Glycosides, 448 2 Digitoxin, 448 2 Digoxin, 448 5 Doxepin, 1278 5 Hydantoins, 1234 5 Imipramine, 1278 5 Ketamine, 720 4 Metoprolol, 249 5 Nortriptyline, 1278 2 Oxtriphylline, 1220 5 Phenytoin, 1234 4 Propranolol, 249 5 Protriptyline, 1278 1 Sibutramine, 1062 2 Theophylline, 1220 2 Theophyllines, 1220 5 Tricyclic Antidepressants, 1278 5 Trimipramine, 1278 1 Warfarin, 85 DHT, see Dihydrotachysterol Di-Gel, see Antacids DiaBeta, see Glyburide Diabinese, see Chlorpropamide Dialume, see Aluminum Hydroxide Diamox, see Acetazolamide Diasorb, see Attapulgite Diazepam, 5 Aluminum Hydroxide, 177 5 Aluminum Hydroxide Magnesium Hydroxide, 177 3 Aminophylline, 207 5 Antacids, 177 4 Atracurium, 891 2 Azole Antifungal Agents, 178 5 Beta Blockers, 179 3 Cimetidine, 182 5 Ciprofloxacin, 203 5 Cisapride, 183 2 Clarithromycin, 196 4 Clozapine, 184 3 Contraceptives, Oral, 186.
Mibefradil belongs to a new class of calcium blockers; unlike traditional calcium blockers, it selectively blocks T-type transient, low-voltage-activated ; calcium channels Welker et al 1998 ; . Mibefradil can thus serve as an oral treatment for hypertension and stable angina pectoris. It dilates the peripheral and coronary vessels, which results in a reduction in arterial pressure and peripheral vascular resistance, and an increase in coronary artery blood flow Welker et al 1998 ; . Mibefradil reduces heart rate dose-dependently and does not cause reflex tachycardia, as is commonly seen with dihydropyridine calcium blockers Welker et al 1998 ; . The recommended dosage is 50 to 100 mg once daily. About 99.5% of mibefradil is bound to plasma proteins, mainly to 1-acid glycoprotein Welker et al 1998 ; . The Vd of mibefradil in the steady state ranges from 130 l to 200 l Dollery 1999b, du Souich et al 2000 ; . Mibefradil exhibits dose- and time-dependent pharmacokinetics that can be explained by partial saturation of the metabolism or by inhibition of mibefradil metabolism by mibefradil itself or by accumulated metabolites du Souich et al 2000 ; . Its t averages 15 h, with a range of about 10 to 38 Dollery 1999b, Welker et al 1998, du Souich et al 2000 ; . Mibefradil is eliminated largely by metabolism, and excreted mainly in the faeces 75% ; , to a lesser extent in the urine 25% less than 3% is excreted unchanged in the urine. The metabolism of mibefradil is mediated by two main pathways, CYP3A4-mediated oxidation and hydrolysis of the ester side-chain. Such hydrolysis produces Ro 40-5966, which is, however, the major plasma metabolite, possessing about 10% of the pharmacodynamic activity of the parent drug Welker et al 1998 ; . A total of some 30 metabolites of mibefradil have been detected Wiltshire et al 1997 ; . In vitro studies on human liver microsomes have shown mibefradil to be a potent inhibitor of CYP3A4 and CYP2D6 Welker et al 1998, Wang et al 1999, Bohets et al 2000 ; . In vivo, mibefradil has increased the total AUC of CYP3A4 substrates cyclosporin and triazolam 2.7-fold and 9-fold, respectively, and enhanced the sedative effects of triazolam Welker et al 1998, Backman et al 1999 ; . In addition, mibefradil raises the plasma concentration of terfenadine and the mean QTc interval, resulting in an increased risk for cardiac arrhythmias Welker et al 1998 ; . Mibefradil also considerably increases plasma concentrations of metoprolol, a substrate of CYP2D6 Welker et al 1998 ; . Besides inhibiting CYP3A4, mibefradil also inhibits P-gp in vitro Wandel et al 2000 ; . However, in humans mibefradil raises plasma concentrations of digoxin only at supratherapeutic levels Siepmann et al 1995, Welker et al 1998. The fda refused and required knoll to apply for a new drug application following proper testing for safety and effectiveness.
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Iabetes is a serious medical condition associated with disability, premature death, and enormous medical costs 1 ; . Arguably more important is the insidious way in which the diagnosis of diabetes afflicts people with worry and despair over the loss of health as well as the burden of self-care. As health care professionals, our recommendations to patients regarding methods and targets of treatment can dramatically influence the quality of patients' lives. The issue at hand is this: Should postprandial glucose PPG ; be routinely measured and treated to a particular target? I will answer this from the perspective of guidelines generally applicable in the medical community, with the recognition that for particular patients, very different approaches could be appropriate. The problem with attempting to answer this question is that there is essentially no direct clinical trial evidence to inform the decision, leaving a great deal to opinion. There are numerous epidemiological studies, such as DECODE Diabetes Epidemiology: Collaborative Analysis Of Diagnostic Criteria in Europe ; , suggesting that 2-h glucose levels 140 mg dl obtained after a 75-g oral glucose load are associated with increased risk of cardiovascular disease CVD ; , in excess of the risk defined by fasting glucose 2 ; . These results have been used as the primary evidence that patients and providers should.
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Reducing health care-associated infection is a high priority for the NHS. The term health careassociated infection is now frequently used instead of hospital-acquired infection, since an increasing amount of treatment and care is taking place in primary and community care facilities.1, 2 The National Institute for Clinical Excellence NICE ; has published a clinical guideline on infection control in primary and community care, which includes standard principles of hand hygiene.3 Hand hygiene is possibly the most important factor in preventing hospital-acquired infection, 1 and it is being increasingly acknowledged that it is also important in community settings. There are few robust studies specifically relating to hand hygiene within primary and community care, and ethical and practical issues make conducting such studies difficult. However, there are some studies of varying quality that confirm the association between hand decontamination and a reduction in the incidence of infection, and expert opinion from guidelines regarding hospital-acquired infection support this. When should hands be decontaminated? The clinical guideline from NICE recommends that hands must be decontaminated immediately before each and every episode of direct patient contact or care, and after any activity or contact that could potentially result in hands becoming contaminated.3 In the community and patients' own homes, the method of hand decontamination will depend largely on what is practical, available and appropriate for the care or treatment being undertaken. However, NICE recommends that: 3 grossly contaminated with dirt or organic material, must be washed with liquid soap and water Hands must be decontaminated, preferably with an alcohol-based handrub unless hands are visibly soiled, between caring for different patients and between different care activities for the same patient. the community, this may involve providing and promoting the appropriate use of alcoholbased handrubs, as this may be the most practical way of improving hand hygiene in such situations. Is this anything new? Health care workers clean their hands less than half as often as they should, and the National Patient Safety Agency has identified poor hand hygiene as a major patient safety issue.4 In December 2003, the Department of Health launched a new drive to ensure that staff follow hand hygiene protocols, with the publication of an action plan to reduce health care-associated infection.2 Several barriers to correct hand hygiene have been identified, such as poor knowledge of guidelines, lack of education, inadequate facilities, lack of time and lack of hand hygiene agents.2 Audit The Department of Health controls assurance standard for infection control has criteria relevant to hand hygiene.5 Although, to date, assessment against this standard has been limited to hospital trusts, the principles apply across the NHS.5 Along with the NICE clinical guideline, it provides useful audit criteria, such as: 3, 5. 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Rifampicin may reduce lercanidipine's plasma levels and therefore the efficacy of lercanidipine may be less than expected. see: Interaction with other medicinal products and other forms of interaction ; . One tablet of Vasodip 10 contains 30 mg lactose. This amount is probably too small to give rise to significant symptoms in patients with lactose intolerance. 1 tablet of Vasodip 20 contains 60 mg lactose and therefore should not be administered to patients with Lapp lactase insufficiency, galactosaemia or glucose galactose malabsorption syndrome. Interaction with other medicinal products and other forms of interaction: Lercanidipine is known to be methabolised by the CYP3A4 enzyme and therefore inhibitors and inducers of CYP3A4 administered concurrently may interact with the metabolism and elimination of lercanidipine. Co-prescription of Vasodip with inhibitors of CYP3A4 e.g. ketoconazole, itraconazole, ritonavir, erythromycin, troleandomycin ; should be avoided see: Contraindications ; . An interaction study with a strong CYP3A4 inhibitor, Ketoconazole, has shown a considerable increase in plasma levels of lercanidipine a 15-fold increase of the AUC and an 8-fold increase of the Cmax for the eutomer S-lercanidipine ; . Cyclosporin and lercanidipine should not be administered together see: Contraindications ; . Increased plasma levels of both lercanidipine and cyclosporin have been observed following concomitant administration. A study in young healthy volunteers has shown that when cyclosporin was administered 3 hours after the lercanidipine intake the plasma levels of lercanidipine did not change, while the AUC of cyclosporin increased by 27%. However, the co-administration of Vasodip with cyclosporin has caused a 3-fold increase of the plasma levels of lercanidipine and a 21% increase of the cyclosporin AUC. Lercanidipine should not be taken with grapefruit juice see: Contraindications ; . As for other dihydropiridines, lercanidipine is sensitive to inhibition of metabolism by grapefruit juice, with a consequent rise in it's systemic availability and increased hypotensive effect. When concominantly administered at a dose of 20 mg with midazolam p.o. to elderly volunteers, lercanidipine's absorption was increased by approximately 40% ; and the rate of absorption was decreased tmax was delayed from 1.75 to 3 hours ; . Midazolam concentrations were not modified. Caution should be exercised when Vasodip is co-prescribed with other substrates of CYP 3A4, like terfenadine, astemizole, class III antiarrhythmic drugs such as amiodarone and quinidine. Co-administration of Vasodip with CYP 3A4 inducers like anticonvulsants e.g. phenytoin, carbamazepine ; and rifampicin should be approached with caution since the antihypertensive effect may be reduced and blood pressure should be monitored more frequently than usual. When Vasodip was co-administered with metoprolol, a -blocker eliminated mainly by the liver, the bioavailability of metoprolol was not changed while that of lercanidipine was reduced by 50%. This effect may be due to the reduction in the. Avoid alcohol while taking metoprolol and ultram. Marketing and sales we initially marketed our pharmaceutical product lines through a contract sales force, for example, toprrol side affect. Metoprolol has no intrinsic sympathomimetic activity, and membrane-stabilizing activity is detectable only at plasma concentrations much greater than required for beta-blockade and valtrex. 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Department of Neurology, University of Bonn, Germany; Department of Immunology, University of Heidelberg, Germany; Institute of Molecular Medicine and Experimental Immunology, University of Bonn, Germany; and Department of Neurology, University of Munster, Munster, Germany Received for publication November 8, 2004. Accepted for publication June 22, 2005. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact and vasotec. ATABRINE IN RHEUMATIC DISEASES 283 Table 1. Mechanisms of Action Antiprostaglandin actions Platelet aggregation inhibition DNA, RNA polymerase inhibition Blocking of LE cell factor Antioxidant effects Antihemolysin activity Neutrophil and lysosome stabilization Na-Ca exchange impedance Hormonal interactions: antagonism of prolactin and insulin Bradykinin and histamine antagonization Antiproliferative and radiation potentiation effects Antimutagenic effects Photochemical blockade Anticholinesterase and sympatholytic actions Depression of immune responsiveness Quinidine-like cardiac actions and reduction of infarct size Antimicrobial activities Sclerosing actions. Q2 An elderly lady presents with a scalp laceration after a syncopal episode. On further questioning, she states that she has had several syncopal episodes in the past week or so. She is on a number of medications, including aspirin and metoprolol. Which of the following abnormalities on her ECG would be least likely to help you in deciding to use electrophysiological studies to investigate the patient? A. B. C. Which of the following diabetes-related neurological problems is most likely to improve with time? A. Diabetic amyotrophy. B. Painful peripheral neuropathy. C. Absent reflexes. Polymorphic ventricular ectopic beats. Paroxysmal atrial fibrillation with a rate of 110 beats per min. Sinus bradycardia. Intermittent second degree heart block during sleep. Significantly prolonged QT interval and verapamil. Missouri based company expects to immediately begin shipping of the mg and mg strengths of the metoprolol succinate extended. ONE of Scotland's most senior doctors has backed a proposed bill that would make mercy killing legal. Dr Gordon Peterkin is the first medical director publicly to support euthanasia. The former family doctor, now medical director at NHS Grampian, has offered written support for a private member's bill to legalise assisted suicide, saying that many modern treatments to keep patients alive were "harmful to patients and disruptive to families". The Scottish parliament bill Dying with Dignity, proposed by Jeremy Purvis, the Liberal Democrat MSP, would allow doctors to help terminally ill adults end their own lives. At present doctors can provide dying patients only with pain relief and face prosecution if they shorten lives. Under the proposed law, expected to be voted on by MSPs next year, any competent terminally ill adult with less than six months to live would be allowed to obtain lethal medication from their doctor. The dose would be self-administered after the patient made two verbal requests to die to their doctor, after another doctor had confirmed their prognosis and after the patient was made aware of alternative treatments. Peterkin responded to a consultation on the bill in a personal capacity, making it clear that he supported the proposals. "Attempts to prolong life at all costs [mean] doctors end up treating people they know are going to die as experimental animals, " he said. "I have had relatives who have been well cared for but overenthusiastically treated, where they could have been more comfortable and dealt with in a more pragmatic and sensible way. "In terms of treating people, you can keep them alive for a long time, we now have more technology to enable us to do that, but individuals end up having a most uncomfortable time. You're simply making patients miserable and to my mind that is not fair and vicoprofen and toprol, for example, generic of toprol.

About eisai inc eisai inc is a us pharmaceutical subsidiary of eisai co, ltd, a research-based human health care hhc ; company that discovers, develops and markets products in more than 30 countries. Unavailability of electrolyte mineral mixture can be attributed to the pharmacist posts that were vacant see Table 6 ; . e. Training and Teamwork: The nurses seem to have an insight into their lack of knowledge and skills, because they mentioned training in the EC protocol as a need. They also emphasised the need for multisectoral approach, such as entitlement to child support grants, foster care grants and disability grants. They did not articulate the problems fully, as they seem not to understand how the basic and underlying causes lead to immediate problems. Puoane, et al. 2001 ; found that long-term sustainable improvement required a team involving paediatric staff, dieticians, pharmacists, kitchen staff and administration and identification of shortcomings. They emphasise that, where appropriate, the team should undergo training to improve their skills and knowledge. Strasser 2000 ; states that the basic competencies knowledge, attitudes and skills ; are needed to meet the challenges. Also new skills are lacking in nurses and the nursing programmes do not seem to respond to this challenge. Radebe 2000 ; claims that the nurses are trained in urban areas and are not trained to work in rural areas and PHC clinics. A study on GMP in Mt. Frere Chopra, et al., 2000 ; found that the main problem of poor GMP was not one of knowledge, but of behaviour. The authors conclude: "The perception of heavy workload and a lack of and vioxx.

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Figure 4. Analysis of mRNA levels in cerebellar granule cells. Cultures were switched to K5 S, and cDNA was prepared from granule cells after 1, 3, 6, or 36 hr. cDNA from 4000 cells was used in a 50 PCR reaction, as described in Materials and Methods. Each transcript was analyzed from at least two different neuronal preparations. A, Representative response of cerebellar granule cells in K5 S medium comprehensive list in Table 1 ; . cyclophilin was typical of genes that decreased. cyclin D1 decreased slightly and then increased to control levels by 36 hr. c-jun increased approximately fivefold during PCD. S-100, a marker for non-neuronal cells, remained relatively constant. B, Quantitation by PhosphorImager analysis of mRNA levels in cerebellar granule cells in K5 S medium.
Baden HP, Champliaud M-F, Sundberg JP, Viel A. 2005. Targeted deletion of the sciellin gene in normal development and maturation. Genesis 42: 219-228. Kennel SJ, Lankford T, Garland M, Sundberg JP, Mirzadeh S. 2005. Biodistribution of 225Ra citrate in mice: Retention of daughter radioisotopes in bone. Nucl Med Biol 32: 859867. Sundberg JP, Peters EMJ, Paus R. 2005. Analysis of hair follicles In mutant laboratory mice. J Invest Dermatol Symp Proc 10: 264-270. Freyschmidt-Paul P, Zoller M, McElwee KJ, Sundberg JP, Happle R, Hoffmann R. 2005. The functional relevance of the type 1 cytokines IFN-gamma and IL-2 in alopecia areata in C3H HeJ mice. J Invest Dermatol Symp Proc 10: 282-283. Beckwith J, Cong Y, Sundberg JP, Elson CO, Leiter EH. 2005. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology 129: 1473-1484. Renninger ML, Seymour R, Lillard JW, Sundberg JP, HogenEsch H. 2005. Increased expression of chemokines in the skin of chronic proliferative dermatitis mutant mice. Exp Dermatol 14: 906-913. Rector A, Van Doorslaer K, Bertelsen M, Barker IK, Olberg RA, Lemey P, Sundberg JP, Van Ranst M. 2005. Isolation and cloning of the raccoon Procyon lotor ; papillomavirus type 1 by using degenerate papillomavirus-specific primers. J Gen Virol 86: 2029-2033. Freyschmidt-Paul P, McElwee KJ, Hoffmann R, Sundberg JP, Kissling S, Hummel S, Vitacolonna M, Kopp-Schneider A, Zoller M. 2005. Reduced expression of interleukin-2 decreases the frequency of alopecia areata onset in C3H HeJ mice. J Invest Dermatol 125: 945-951. Mikaelian I, Hovick M, Silva KA, Bursenski LM, Shultz LD, Ackert-Bicknell CL, Cox GA, Sundberg JP. 2006. Expression of terminal differentiation proteins defines stages of mouse mammary gland development. Vet Pathol 43: 36-49. Bikle DD, Elalieh H, Chang S, Xie Z, Sundberg JP. 2006. Development and progression of alopecia in the vitamin D receptor null mouse. J Cell Physiol 17: Epub ahead of print. Gould DB, Phalan FC, van Mil SE, Sundberg JP, Vahedi K, Massin P, Bousser MG, Heutink P, Miner JH, Tournier-Lasserve E , John SWM. 2006. Role of COL4A1 in small-vessel disease and hemorrhagic stroke. N Engl J Med 354: 1489-1496. Seymour RE, Sundberg JP, HogenEsch H. Development of lymphoid organs in immunodeficient mutant mice. Vet Pathol, in press. Books, Book Chapters, and Reviews Sundberg JP, Ichiki T. 2005. Handbook on Genetically Engineered Mice, Francis and Taylor, Boca Raton, Fla. Sundberg JP, Bult C. 2005. Professional Use of Mutant Laboratory Mice in Research. In: Handbook on Genetically Engineered Mice, Sundberg JP, Ichiki T, [eds], CRC Press, Boca Raton, Fla., pp. 185-210. Sundberg JP, Ichiki T. 2005. Phenotyping Postpartum Mutant Laboratory Mice and Determining Their Value as Animal Models for Human Diseases. In: Handbook on Genetically Engineered Mice, Sundberg JP, Ichiki T, [eds], CRC Press, Boca Raton, Fla., pp. 211-222.

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