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Contributions to a part of a book on the Internet generic 10mg aristocort with mastercard, such as a table or fgure order 4mg aristocort visa, may be cited as individual items order aristocort cheap online. Continue to Citation Rules with Examples for Contributions to Books on the Internet generic 4 mg aristocort fast delivery. Citation Rules with Examples for Contributions to Books on the Internet Components/elements are listed in the order they should appear in a reference. An R afer the component name means that it is required in the citation; an O afer the name means it is optional. Author (R) | Author Afliation (O) | Title (R) | Connective Phrase (R) | Book Information (R) | Date of Citation (R) | Location (Pagination) (R) | Availability (R) | Language (R) | Notes (O) Books and Other Individual Titles on the Internet 1467 Author of a Contribution to a Book on the Internet (required) General Rules for Author • List names in the order they appear in the text • Enter surname (family or last name) frst for each author • Capitalize names and enter spaces within surnames as they appear in the document cited on the assumption that the author approved the form used. Tis rule ignores some conventions used in non-English languages to simplify rules for English-language publications. Books and Other Individual Titles on the Internet 1469 Box 94 continued from previous page. Names in non-roman alphabets (Cyrillic, Greek, Arabic, Hebrew, Korean) or character-based languages (Chinese, Japanese). Romanization, a form of transliteration, means using the roman (Latin) alphabet to represent the letters or characters of another alphabet. Tis rule ignores some conventions used in non-English languages to simplify rules for English-language publications. Books and Other Individual Titles on the Internet 1471 Box 98 continued from previous page. An organization such as a university, society, association, corporation, or governmental body may serve as an author. International Union of Pure and Applied Chemistry, Organic and Biomolecular Chemistry Division. American College of Surgeons, Committee on Trauma, Ad Hoc Subcommittee on Outcomes, Working Group. American Academy of Pediatrics, Committee on Pediatric Emergency Medicine; American College of Emergency Physicians, Pediatric Committee. Tis rule ignores some conventions used in non-English languages to simplify rules for English-language publications. Books and Other Individual Titles on the Internet 1473 Box 99 continued from previous page. Separate the surname from the given name or initials by a comma; follow initials with a period; separate successive names by a semicolon. Standard reference to a contributed chapter of an Internet book 1474 Citing Medicine 2. Contribution to an Internet book with optional full frst names for authors and editors 3. Contribution to an Internet book with authors having a family designation of rank 5. Contribution to an Internet book with author names having a particle or prefx (give as found in the publication) 6. Books and Other Individual Titles on the Internet 1475 Box 101 continued from previous page. If you abbreviate a word in one reference in a list of references, abbreviate the same word in all references. Marubini E (Istituto di Statistica Medica e Biometria, Universita degli Studi di Milano, Milan, Italy), Rebora P, Reina G. Tis rule ignores some conventions used in non-English languages to simplify rules for English-language publications. Books and Other Individual Titles on the Internet 1477 Box 103 continued from previous page. Moskva becomes Moscow Wien becomes Vienna Italia becomes Italy Espana becomes Spain Examples for Author Affiliation 7. Contribution to an Internet book with author afliation included Title of a Contribution to a Book on the Internet (required) General Rules for Title • Enter the title of the chapter or other contribution as it appears in the original document, in the original language • Capitalize only the frst word of a title, proper nouns, proper adjectives, acronyms, and initialisms • Use a colon followed by a space to separate a title from a subtitle unless some other form of punctuation (such as a question mark, period, or an exclamation point) is already present 1478 Citing Medicine • Follow non-English titles with a translation whenever possible; place the translation in square brackets • End a title with a period unless a question mark or exclamation point already ends it Specific Rules for Title • Titles not in English • Titles in more than one language • Titles containing a Greek letter, chemical formula, or other special character Box 105. Diagnostika i kompleksnoe lechenie osnovnykh gastroenterologicheskikh zabolevanii: klinicheskie ocherki. Tis rule ignores some conventions used in non-English languages to simplify rules for English-language publications. Books and Other Individual Titles on the Internet 1479 Box 105 continued from previous page. Base molecular de la expresion del mensaje genetico [Molecular basis of gene expression]. Diagnostika i kompleksnoe lechenie osnovnykh gastroenterologicheskikh zabolevanii: klinicheskie ocherki [Diagnosis and complex treatment of basic gastrointestinal diseases: clinical studies]. If a chapter or another contribution is presented in two or more equal languages, as ofen occurs in Canadian publications: • Give all titles in the order in which they are found on the title page or opening screens • Place an equals sign with a space on either side between the titles Example: Box 106 continues on next page... Le genome: avancees scientifques et therapeutiques et consequences sociales = Te genome: scientifc and therapeutic developments and social consequences. Books and Other Individual Titles on the Internet 1481 Box 107 continued from previous page. Contribution to an Internet book with title beginning with a lower-case letter or containing a special symbol or character 10. Contribution to an Internet book with a non-English title Connective Phrase for a Contribution to a Book on the Internet (required) General Rules for Connective Phrase • Place a space and the word "In" afer the title of the contribution • Follow "In" with a colon and a space Examples for Connective Phrase 1. Contribution has a date of publication or date of update/revision that difers from the book as a whole. Contributions may be published with individual dates separate from the date of the book as a whole or may be updated or otherwise revised separately from book as a whole. When this occurs: • Give a separate date of publication and/or date of update/revision afer the title for the contribution Box 108 continues on next page... Contributed paper in a conference proceedings on the Internet Date of Citation for a Contribution to a Book on the Internet (required) General Rules for Date of Citation • Always include the date the contribution to a book was seen on the Internet • Include the year month and day in that order, such as 2006 May 5 • Use English names for months and abbreviate them using the frst three letters, such as Jan • If a date of update/revision is given, place the date of citation afer it and follow both dates with a right square bracket • If no date of update/revision is given, place citation date information in square brackets • End date information with a period placed outside the closing bracket Books and Other Individual Titles on the Internet 1483 Specific Rules for Date of Citation • Both a date of update/revision and a date of citation Box 109. Various words are used to show that the content of a contribution a book has been changed. When this occurs, give the total number of pages of the part you are to citing, placed in square brackets, such as [5 p. Books and Other Individual Titles on the Internet 1485 Box 112 continued from previous page. If the entire contribution is a video clip, videocast, or podcast: • Enter the word Video, Videocast, or Podcast followed by a colon and a space • Give extent as the number of minutes needed to view/listen • Abbreviate minutes to min. Contribution to an Internet book with location (pagination) expressed as standard page numbers 16. Hypertextbook of regional anaesthesia for obstetrics: an international perspective [Internet]. Late-stage breast cancer among women with recent negative screening mammography: do clinical encounters ofer opportunity for earlier detection? Health care systems as research platforms: the cancer research network Box 119 continues on next page... System requirements describe the particular sofware and hardware needed to view the contribution to the book. Books and Other Individual Titles on the Internet 1491 Box 121 continued from previous page. Contributed chapter in one volume of a multivolume book Examples of Citations to Contributions to Books on the Internet 1. Contribution to an Internet book with optional full first names for authors and editors Andreef, Michael; Goodrich, David W. Contribution to an Internet book with optional limit to the number of authors Mouchawar J, Taplin S, Ichikawa L, et al. Late-stage breast cancer among women with recent negative screening mammography: do clinical encounters ofer opportunity for earlier detection? Health care systems as research platforms: the cancer research network [Internet]. Late-stage breast cancer among women with recent negative screening mammography: do clinical encounters ofer opportunity for earlier detection?

Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production cheap aristocort generic. Low serum cobalamin levels occur frequently in the acquired immune deficiency syndrome and related disorders 10 mg aristocort fast delivery. Severe deficiency of 1 purchase cheapest aristocort,25-dihydroxyvitamin D3 in human immunodeficiency virus infection: association with immunological hyperactivity and only minor changes in calcium homeostasis aristocort 40mg amex. Suppression of human immunodeficiency virus type 1 viral load with selenium supplementation: a randomized controlled trial. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology 1997; 15: 370–374. Therapeutic application of zinc in human immunodeficiency virus against opportunistic infections. Studies on lipoate effects on blood redox state in human immunodeficiency virus infected patients. Carnitine in human immunodeficiency virus type 1 infection/acquired immune deficiency syndrome. Protective actions of L-carnitine and acetyl-L-carnitine on the neurotoxicity evoked by mitochondrial uncoupling or inhibitors. Detecting life-threatening lactic acidosis related to nucleoside-analog treatment of human immunodeficiency virus-infected patients, and treatment with L-carnitine. Three inhibitors of human type 1 immunodeficiency virus: long terminal repeat, directed gene expression, and virus replication. Proceedings of the National Academy of Sciences of the United States of America 1993; 90: 1839–1841. Comparison of systemic availability of curcumin with that of curcumin formulated with phosphatidylcholine. Journal of the American Academy of Child and Adolescent Psychiatry 2001; 40: 83–90. The severity of liver fibrosis is associated with high leptin levels in chronic hepatitis C. Effects of zinc deficiency on ethanol metabolism and alcohol and aldehyde dehydrogenase activities. Proceedings of the Society for Experimental Biology and Medicine 1977; 154: 146–150. Endocrine control of ethanol intake by rats or hamsters: relative contributions of the ovaries, adrenals and steroids. Effect of alcohol consumption of blood antioxidant nutrients and oxidative stress indicators. Role of selenium depletion in the etiopathogenesis of depression in patients with alcoholism. A mechanism of the acute ethanol-induced fatty liver and the modification of liver injury by antioxidants. American Journal of Pharmacy and the Sciences Supporting Public Health 1966; 15: 50–63. Ameliorating effects of carnitine and its precursors on alcohol-induced fatty liver. Changes in plasma amino acid patterns in chronic alcoholic patients during ethanol withdrawal syndrome: their clinical implications. Relationship between changes in plasma amino acids and depression in alcoholic patients. Hepatic, metabolic, and nutritional disorders of alcoholism: from pathogenesis to therapy. Ethanol-ascorbate interrelationship in acute and chronic alcoholism in the guinea pig. Proceedings of the Society for Experimental Biology and Medicine 1984; 177: 262–271. Adequacy or deprivation of dietary selenium in healthy men: clinical and psychological findings. Disproportionate suicidality in patients with comorbid major depression and alcoholism. Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status. Thiamine deficiency as predisposition to, and consequence of, increased alcohol consumption. Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. The role of acetaldehyde in mediating the deleterious effect of ethanol on pyridoxal 5-phosphate metabolism. Cumulative excess urinary excretion of folate in rats after repeated ethanol treatment. Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics. Ethanol consumption alters electroretinograms and depletes neural tissues of docosahexaenoic acid in rhesus monkeys: nutritional consequences of a low n-3 fatty acid diet. Acute effects of moderate alcohol consumption on blood pressure and plasma catecholamines. An extract of the Chinese herbal root kudzu reduces alcohol drinking by heavy drinkers in a naturalistic setting. A pilot study exploring the effect of kudzu root on the drinking habits of patients with chronic alcoholism. Randomized controlled trial of silymarin treatment in patients with cirrhosis of the liver. Insulin resistance and Alzheimer’s disease pathogenesis: potential mechanisms and implications for treatment. Nutraceutical properties of Mediterranean diet and cognitive decline: possible underlying mechanisms. Mediterranean diet, inflammatory and metabolic biomarkers, and risk of Alzheimer’s disease. Oxidative stress and Alzheimer’s disease: dietary polyphenols as potential therapeutic agents. Phenolic compounds prevent Alzheimer’s pathology through different effects on the amyloid-beta aggregation pathway. Health benefits of fruit and vegetables are from additive and synergistic combinations of phytochemicals. Phenolic compounds prevent Alzheimer’s pathology through different effects on the amyloid-beta aggregation pathway. Consumption of grape seed extract prevents amyloid-beta deposition and attenuates inflammation in brain of an Alzheimer’s disease mouse. Grape derived polyphenols attenuate tau neuropathology in a mouse model of Alzheimer’s disease. Pharmacokinetics and tissue distribution of 14C-labeled grape polyphenols in the periphery and the central nervous system following oral administration. L-3-n-butylphthalide improves cognitive impairment and reduces amyloid-beta in a transgenic model of Alzheimer’s disease. The Women’s Health Initiative Memory Study: findings and implications for treatment. Association between hormone replacement therapy and dementia: is it time to forget? Hormone replacement therapy to maintain cognitive function in women with dementia. Interaction of aluminum with paired helical filament tau is involved in neurofibrillary pathology of Alzheimer’s disease. Aluminum and lead absorption from dietary sources in women ingesting calcium citrate. Dementias: the role of magnesium deficiency and hypothesis concerning the pathogenesis of Alzheimer’s disease. Dietary antioxidants and cognitive function in a population-based sample of older persons.

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In contrast to other ions safe 10 mg aristocort, only a small fraction of filtered magnesium (15–20%) is reabsorbed Most laboratories in the United States report the in the proximal tubule (Fig purchase cheap aristocort online. In immature animals discount aristocort online amex, results of body fluid magnesium concentration in units the proximal tubule accounts for 60–70% of magne- of milliequivalents per liter or milligrams per deciliter discount aristocort 40 mg overnight delivery, sium ions (Mg2+) reabsorption [26]. Paracellular transport lineary rising with intraluminal tor determining renal magnesium handling. The resulting lumen positive (under normal circumstances) voltage is expected to drive the Mg2+ be passive and paracellular, driven by the favorable electrical gradient resulting from the reabsorption of reabsorption even against the concentration gradient. Paracellular magnesium reabsorption is facilitated by the tight junction protein include transepithelial voltage and permeability of the paracellin-1, which also serves as a main route for paracellular pathway. Samsonov a paracellular pathway can be diminished as a result of thick ascending limb paracellin-1 mutations (see Sect. Paracellular reabsorption of magnesium and Hypomagnesemia - No change - calcium is driven by lumen-positive transcellular reabsorption of. Bone, the major somal recessive disorder characterized primarily by 2+ intracellular Mg reservoir, does not readily exchange intestinal malabsorption of Mg (see Sect. Compared with normal individuals these or decreased intestinal absorption can be compensated patients have lower threshold for magnesium urinary only by increased renal reabsorption. Thus, patients treated with intra- The driving force for the exchange is a high- venous fluids containing dextrose and sodium chloride sodium concentration gradient between extracellu- –1 –1 may develop hypomagnesemia rather quickly, espe- lar (140 meq L ) and intracellular (10–15 meq L ) + 2+ cially in the presence of tubular damage and the inabil- compartments, which favors Na entry and Mg exit. Second, the human body has no Because Mg2+ transport in the distal tubule operates good protection against hypermagnesemia in the pres- close to its maximal capacity, it is believed that the 2+ ence of impaired renal function. However, some evidence suggests that this segment regulates the final urine magnesium excretion. Amiloride, a potassium and magnesium sparing diuretic, causes hyperpolari- Hypomagnesemia is a common problem occurring in zation of the membrane voltage that increases the 7–11% of hospitalized patients and in as many as 60% driving force for Mg2+ entry. Interestingly, thiazide- ciency can be demonstrated in up to 40% of patients type diuretics have little effect on Mg2+ handling. However, both human studies and animal cardiac, neuromuscular, and metabolic abnormali- micropuncture studies fail to demonstrate increase ties; however, cardiac and neurological symptoms can in Mg2+ excretion after treatment with thiazide diu- also frequently be attributed to coexisting metabolic retics [47]. These findings are puzzling when com- abnormalities such as hypokalemia or hypocalcemia. Magnesium is a cofactor in all reactions that inhibition of carbonic anhydrase [48]. The test is Hypocalcemia is present in about half of the patients performed by collecting twice 24-h urine for magne- with severe hypomagnesemia. Multiple mechanisms, sium – one collected before and second after the admin- contributing to hypocalcemia, have been identified. A reduced outward K + nificant amounts, hypomagnesemia is almost never gradient diminishes K efflux during repolarization observed in normal individuals even on a strict diet. Tonic–clonic generalized fatty acids in the intestinal lumen combine with cations convulsions were described as a first manifestation of (saponification) and form nonabsorbable soaps. This hypomagnesemia and sometimes can be triggered by process can interfere with Mg2+ absorption [25, 34]. Data from animal studies suggest that effect of Congenital defect of magnesium absorption has magnesium deficiency on brain neuronal excitability been recently described. Magnesium deficiency can be induced by either High doses of enteral magnesium are required to decreased intake or increased losses. Because bone keep serum magnesium and calcium levels close to magnesium reservoir does not readily exchange normal range [38, 45]. Decreased intake of mag- tract have much higher magnesium concentrations (up nesium can be secondary to diminished amount to 16 mg dL–1) than from the upper gastrointestinal of enteric Mg2+ delivery or reduced absorption tract. Magnesium wasting can be via gastroin- fistulas, iliostomy or gastric drainage rarely develop testinal or renal route. In contrast, chronic diarrhea and diagnosis of hypomagnesemia will be discussed in short bowel syndrome can be associated with hypo- the Sect. Patients with bone formation, which is thought to be responsible for severe burns can be prone to develop hypomagnesemia Ca2+ and Mg2+ sequestration into bone tissue [17]. In this condition, rapid cellular uptake of tion of sodium and chloride in this segment promotes water, glucose, potassium, phosphorus, and magne- urinary loss of magnesium. Expansion of extracellular Chapter 5 Abnormalities in Magnesium Metabolism 77 fluid volume as a result of hyperaldosteronism or inap- in both preclinical and clinical studies. All clinically propriate antidiuretic hormone secretion can result in available aminoglycosides including gentamicin, mild hypomagnesemia. Also topically administered for extensive burn postobstructive, osmotic diuresis, and recovery from injury, neomycin can cause classical metabolic triad postischemic injury of transplanted kidney [1]. Even Hypercalcemia symptomatic hypomagnesemia as a complication of Hypercalcemia directly induces renal Mg2+ wasting, accepted 3–5 mg kg–1 day–1 standard dose regimen is the effect that is clearly observed in patients with relatively rare; asymptomatic hypomagnesemia can malignant bone metastases [5]. Nephrotoxicity is a well-appreciated com- Diuretics plication of cisplatin toxicity [3]. Some patients may develop per- syndrome do not cause significant hypermagnesuria manent tubular damage manifesting with hypoka- and hypomagnesemia (see Sect. Carboplatin, an analog of cisplatin, cations can induce specific tubular defect resulting in appears to be less nephrotoxic and rarely causes acute hypermagnesuria. Prospective study of 651 Aminoglycosides cause tubular damage that typi- pediatric patients treated with either cisplatin or car- cally presents with hypokalemia, hypocalcemia, and boplatin in combination with ifosfamide demonstrated hypomagnesemia [11, 24, 34, 40]. In all groups, continuation of the antibiotic treatment and persist for the frequency of hypomagnesemia was decreasing several months. Most reported adult patients who were during the follow-up period of 2 years, but serum mag- treated with high total dose of aminoglycosides had nesium remained lower in platinum-treated patients in normal therapeutic levels suggesting that cumulative the end of the study [43]. However, normal cumulative dose does jor side effect of this potent antifungal medication. Mg2+ vary from asymptomatic cases to generalized convul- loss does not correlate with trough cyclosporine levels sions in early childhood. Laboratory findings include [34], most likely, because of poor correlation between hypermagnesuria, hypomagnesemia, and hypocalciuria cyclosporine trough levels and area under the curve without any other electrolyte abnormalities. In contrast, tacrolimus trough level is a good a genetic locus in the autosomal recessive form has predictor of the drug area under the curve [15], and not been yet identified, in the autosomal dominant tacrolimus-induced magnesium urine loss correlates form a locus was mapped to chromosome 11q23. Nephrocalcinosis and renal stones resulting from hypercalciuria are the Inherited Tubular Defects of Magnesium Handling major clinical findings. Nephrocalcinosis-related renal Bartter syndrome includes a group of inherited disor- insufficiency, distal acidification, and concentrating ders characterized by chloride wasting, hypo-kalemic defects have been also described. This syndrome Affected children usually present with failure to thrive is also associated with frequent ocular abnormalities in infancy or early childhood. Classic Bartter syndrome including corneal calcifications, choreoretinitis, kera- is caused by inactivation mutation of gene coding for toconus, and macular coloboma. Paracellin-1 is a member of the claudin or Barttin, are rarely associated with disturbances of family of tight junction proteins, which is expressed magnesium homeostasis [33, 39]. Paracellin-1 is also Gitelman’s syndrome is a variant of Bartter syn- known as claudin-16; both names are used in the litera- drome characterized by potassium and magnesium ture that can be confusing. Paracellin-1 gene expression is also shown patients and present after the age of 6 years with in cornea and retinal epithelium in animals explaining metabolic abnormalities including mild hypokalemic the link with ocular abnormalities observed in some metabolic alkalosis, hypomagnesemia, and hypocal- patients [34, 39, 42]. Some patients can be asymptomatic and oth- Autosomal dominant hypocalcemia results from ers complain of transient episodes of weakness, tetany, activating mutation of calcium-sensing receptor. Normal values of urine mag- nesium to creatinine ratio in different age groups are 5. In contrast to other electrolytes, the plasma magnesium concentration Monitoring of magnesium status becomes a routine is not always a routine screening blood test. It is reason- nutrition should contain magnesium; otherwise, these able to perform serum magnesium screening in most patients are prone to develop hypomagnesemia. Hypomagnesemia is defined most patients, hypomagnesemia can be prevented as a decrease in serum Mg2+ concentration to levels less by sufficient daily magnesium supplementation than 1. Can the for example, due to low intake and increased gastroin- etiologic factor(s) be withdrawn or ameliorated? Is the patient symptomatic with regard to magne- remains unclear, the differential diagnosis between renal sium depletion? Furthermore, since plasma magnesium 1–10 years 150–250 mg concentration is the major regulator of magnesium 11–18 years 300–400 mg renal handling, acute rise in magnesium concentration >18 years 300–400 mg results in hypermagnesuria with loss of up to 50% of infused magnesium [1]. Therefore, slow continuous Pregnant/lactating +150 mg intravenous infusion over 24 h is effective and safe.

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These2 3 2 2 5 Acid–Base 65 diffuse through the aquaporin channels into the cytosol buy aristocort 15mg otc. There buy discount aristocort 4mg, again mediated by carbonic anhydrase order aristocort 40 mg free shipping, the reaction is reversed and hydrogen and bicarbonate ions are formed again aristocort 15 mg amex. Chloride reabsorption has three main routes: (1) passive+ − 3 due to the electrochemical concentration gradient, (2) active by chloride channels and (3) coupled through various chloride-anion exchangers. Depending on the acid– base status, the different components are either up regulated or down regulated. In alkalosis, chloride excretion is less due to down regulation of pendrin and band 3 protein. As a reaction type B-cells will change and become type-A cells in order to try to increase the hydrogen secretion. Since distal bicarbonate reabsorption is still possible, plasma bicarbonate is normally slightly decreased and blood pH low normal. In the absence of ammonium, less hydrogen can be buffered and thus less hydrogen can be excreted, causing an acidosis. Causes of aldosterone defciency include Addison’s disease, congenital adrenal hyperplasia and drugs inhibiting aldosterone synthesis. Causes of aldosterone resistance include congenital causes, such as pseu- dohypoaldosteronism type 1 and 2 and acquired causes, such as interstitial nephrop- athies and drugs. These start to develop when the glomerular fltration rate is less than 20–25 % of normal. Conclusion Stewart’s strong ion approach, Siggaard-Andersen’s standard base excess approach and the Henderson-Hasselbalch based bicarbonate centered approach are popular frameworks for understanding acid–base disorders in the critically ill. Basic concepts, views of renal acid–base handling and clinical application of these methods were discussed in this chapter. Provided that hypoalbuminemia is corrected for in the latter two, all methods are mathematically compatible and may perform equally well in clinical practice, especially in uncomplicated acid– base disorders. However, if acid–base disorders become increasingly complex, which is the case in many critically ill patients, Stewart’s approach may be superior. Although 5 Acid–Base 67 considered diffcult, this method disentangles and quantifes the various factors responsible for complex mixed acid–base disorders, thus arguably providing the best overview. In addition, by explicitly clarifying the relationship between elec- trolyte disorders and acid–base physiology, the Stewart approach helps to demys- tify the effects of resuscitation fuids on acid–base balance. Our understanding of renal electrolyte handling may need to be revised as a result of the principles of the physiochemical approach. Key Messages • Three approaches to acid–base disorders are in common use: The bicar- bonate centered, base excess and the Stewart approach. All methods are mathematically compatible provided that appropriate corrections are used for the frst two. However, the Stewart approach may be superior in terms of versatility and improved understanding of complex acid–base disturbances. Acidosis in kidney failure is complex and also includes accumulation of weak acids such as phosphate. Our understand- ing of renal electrolyte handling may need to be revised in the context of the Stewart approach. Strong ions, weak acids and base excess: a simplifed Fencl- Stewart approach to clinical acid–base disorders. Accumulating evidence suggests that acute injury and dysfunction to the kidney can incite and propagate cardiac, pulmonary, gastrointestinal, and neurologic injury and dysfunction through a host of mechanisms. Our understanding of the pathophysiological mechanisms underlying this kidney-organ “crosstalk” remains incompletely understood; however, it is likely a complex interaction of patient-specific susceptibilities (i. This chapter will provide a broad overview of the fundamentals of kidney-organ interactions. Importantly, cardiac and kidney disease frequently coexist and together can synergistically modify the risk of major morbid- ity and premature death and translate into excessive health services use. The “car- diorenal syndrome” is generally characterized by the presence of pathophysiological organ “crosstalk” between the heart and the kidneys, whereby an acute or chronic injury or decompensation in the function of one organ can precipitate injury or dys- function to the other. A large body of literature from observational studies and clini- cal trials has clearly shown that acute/chronic heart disease can directly contribute to and/or accelerate acute/chronic worsening of kidney function and vice versa. Recently, a consensus definition and classification scheme for the cardiorenal syn- drome was proposed to help standardize its nomenclature with the aim to better understand its underlying pathophysiological mechanisms, epidemiology, and ther- apeutic approaches. This classification scheme proposed five distinct “cardiorenal” syndrome subtypes (Table 6. These subtypes are characterized by important heart-kidney interactions that share a pathophysiological basis, however, have unique discriminating features, in terms of predisposing or precipitating events, risk identification, natural history, and outcomes. In this section, we will focus on the two subtypes of cardiorenal syndrome most likely to be encountered in critical care. The reported incidence is highly variable depending on the population at risk being eval- uated and the type of procedure performed (i. Injury and/or dysfunction in either or both of these organ systems can directly incite or exacerbate injury and/or impairment in the other. This decrement in kidney function can precipitate clinically important and adverse physiological consequences on the normal function of numerous organ systems, in particular the lung [1]. The accumulation of uremic compounds is known to contribute to lung inflammation and injury and has been termed uremic pneumonitis. Expansion of extracellular volume can contribute to increased pulmonary capillary hydrostatic pressure. This coupled with alterations to pulmonary microvascular per- meability and reduced serum oncotic pressure can predispose to rapid increases in extravascular lung water [13]. Naturally, this organ crosstalk and associated clinical complications may be aggravated in critical illness due to concurrent widespread systemic inflammation (i. Abnormalities in gas exchange are common among critically ill patients with lung injury. These patients often receive supplemental oxygen, noninvasive ventila- tory support, or invasive mechanical ventilation when respiratory failure ensues, with the aim of correcting hypoxemia and restoring near-normal gas exchange. The combined impact of hypoxemia and hypercapnea may act synergistically to impair kidney function [24]. The mechanical disruption of the alveolar-capillary barrier from excessive pressure-volume loading during positive pressure ventilation can induce the release of local inflammatory mediators into the systemic circulation [25]. Further, higher intrarenal vascular resistance (organ compres- sion) shunts blood away from the kidneys. Because the kidney is an encapsulated organ, a pressure rise in the venous system translates into a higher renal interstitial and Bowman’s capsular pressure, directly impeding glomerular filtration [36 , 37]. It has been clearly established that bacterial fermentation processes in the large intestines are an impor- tant source of tightly protein-bound toxins such as p-cresyl sulfate and indoxyl sul- fate [40]. Because of this protein binding, such toxins are difficult to clear from the circulation, even by means of hemodialysis [41]. They may accelerate kidney dys- function, and plasma levels are correlated to all-cause mortality [42, 43]. This offers a strong rationale for targeting gut microbiota and toxin production in the bowel compartment with future therapies. In normal circumstances, the gut has an important barrier function, preventing entrance of toxins and microorganisms into the systemic circulation. Indeed, it has been shown that the intestinal morphology, permeability, and function are substan- tially altered in heart failure [45, 46]. Consequently, leakage of lipopolysaccharides 6 Kidney-Organ Interaction 77 in the systemic circulation may cause further hemodynamic compromise leading to a detrimental vicious cycle [44 , 47]. Orthotopic liver transplantation is the best current treatment and leads to a gradual recovery of renal function in the vast majority of patients. A more thorough under- standing of kidney-organ interactions in the abdominal compartment may hopefully lead to new therapeutic targets to better preserve renal function in critically ill patients. Both organs play a role in regulating sodium and water balance in the body and visceral sympathetic nervous system activity. Clinically examine patients and determine volume status, and review daily weights and serial estimations of fluid intake and output charts, then check serum osmolality, hematocrit, urea, creatinine, and urate and urinary osmolality and electrolytes.

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Other studies have used more typical postural measures to assess the at- tentional demands of postural control discount aristocort 4mg visa. Results similarly suggest a decline in postural stability associated with demanding cognitive tasks (84 buy generic aristocort 4 mg line, 85 order generic aristocort line, 86) 4mg aristocort free shipping. Dual task interference on postural control can be observed in Parkin- sonian patients during performance of cognitive as well as motor tasks (87); the balance deterioration during dual task performance was signifi- cantly enhanced in patients with history of prior falls. Simultaneously, the tensor fasciae latae is inhibit- ed on the stance limb and activated on the swing limb. This pattern would increase the swing hip abductor moment and decrease the stance hip ab- ductor moment, resulting in a momentary loading of the swing limb and unloading of the stance limb. After gait initiation and when walking in normal conditions (no actu- al constraints), adult subjects exhibit a particular stable gait pattern, which is very reproducible from stride to stride, trial to trial but also over days. This rhythmic pattern implies the alternative, out of phase movement of the two legs. The gait cycle is the walking unit defined as the time interval between two successive identical body configurations, in general heel con- tact or heel strike. The gait cycle is divided in two phases: a stance phase – simple or double stance – and a swing phase. Stance and swing durations last about 60% and 40% of the cycle duration, respectively. With increase in body velocity, the stance duration substantially decreases whereas the swing du- ration hardly changes. As a consequence, the duration of the double stance phase significantly decreases with speed increment and even vanishes when switching from walking to running. The stride length linearly increas- es with speed increment until the speed of 2 m/s. Contrary to most mammals, which walk on four legs with the trunk roughly parallel to the ground, humans walk erect on two legs. A pen- dulum-like movement results, which converts ki- netic energy (Ec) into gravitational potential en- ergy (Ep), and inversely, thereby increasing gait efficiency (95, 96) (Fig. Interestingly, model- based studies demonstrated that the human biomechanical system shows a natural propen- sity for locomoting on earth (97). Pendulum-like bipedal locomotor movements are naturally un- movement of the body during stable, in particular in the medio-lateral plane gait. Balance of the trunk and swing leg about the supporting hip is maintained by an active hip abduction moment, which recognises the contribution of the passive accelerational moment, and counters a large destabilizing gravitational moment. Furthermore, bipedal compared to quadrupedal walking implies a dramatic re-organization of patterns of muscle action in order to propel the two-legged body forward while ensuring equilibrium. The motor pat- tern for quadrupedal locomotion consists in a basic alternative activation of extensor (stance) and flexor (swing) muscles. In turn, during human walking, a mixture of extensor and flexor muscles is activated, in particu- lar around the time of heel contact to stiffen the leg and roll over the stance foot. Throughout the remaining stance phase, soleus and gastrocnemii muscles near-solely contribute to producing the necessary energetic flux for propelling the body forward while ensuring ground support (97). Human locomotion along a straight path thus requires a complex se- quence of muscle activation to displace the two legs and the body forward while maintaining balance. However, goal-directed locomotion, such as en- countered in everyday life, often requires steering along curved paths. The inherently unstable bipedal gait becomes critical during curve-walking, as shown by turning difficulties in aged or diseased people (102, 103). Left graph: the horizontal distance between the feet and the body centre of mass changes during curve-walking. The distance decreases for the inner foot (grey symbols) and increases for the outer foot (open symbols), as a function of the curve tightness (change in heading). Right graph: the more tight is the curved trajectory, the larger is the path cov- ered by the outer foot with respect to the inner one. In addition, many temporal and spatial features of the movement of the inner and outer legs become asymmetric. Turn-related adaptations of gait parameters include ever-increasing diver- gences in stance duration, stride length, and foot rotations between the in- ner and outer leg (106), and are mirrored in limb-dependent tuning of mus- cle activity patterns (107). Implementation of a curve trajectory in walking humans thus requires the central nervous system to substantially accom- modate gait characteristics to curve tightness in order to fulfil complex bal- ance and propulsion requirements. Curve-walking may thus provide the ap- propriate context for clinical assessment of gait disorders (108). Neural control of locomotion Neural organisation of the act of progression is based on an interac- tion between subtle supraspinal regulation and basic central and periph- eral elements. Pattern is used in a broad sense to indicate alternating activity in groups of flexors and extensors. After gait initiation, afferents deliver movement-related information to spinal and supraspinal levels. The second role is a tim- ing function (phase-dependent modu- lation) whereby the sensory feedback provides information to ensure that the motor output is appropriate for the biomechanical state of the moving body part in terms of position, direc- tion of movement, and force. Golgi tendon organ; Ib, group Ib affer- Supraspinal centres act in concert ent fibres; Int. In particular, ing location, the Ib inhibition turns into the brainstem neural centres and cere- excitation, and the Ia excitation is being bellum activate the spinal locomotor depressed by presynaptic inhibition. Cortical structures control skilled locomotion when environmental constraints require subtle adaptation of lower limb trajectory (111). Despite this tripartite organisa- tion of the walking system has clearly been demonstrated in vertebrates, no conclusive demonstration of such a control scheme has been provided in humans so far (112). Nevertheless, rhythmic activity is very rare after complete transection of the spinal cord (115). Afferent stimulation or neurotransmitter injection has to be pro- vided to the spinal cord to elicit stepping. By varying the level of transection of the neural ax- is, it was shown that the region for initiation of locomotion is located in the brain stem, at supraspinal level (117). There are clinical studies sug- gesting the existence of similar areas in adult humans (118). Influence of sensory afferent input on locomotor activity Results of studies involving deafferentation and paralysis unequivo- cally demonstrate that the nervous system in mammals is capable of gen- erating rhythmic motor output in the absence of peripheral feedback (119). In humans, the question of the specific role of the various sensory modalities in the reflex control of locomotion is still open: for example, functional loss of leg afferent fibres due to peripheral neuropathy does not always lead to major alteration in the gait pattern. Vibratory tendon stimulation is known to selectively recruit spindle primary afferent fibres (see above): vibration of soleus muscle would therefore disturb organisa- tion and execution of walking, especially if spindles fire continuously and subjects are blindfolded. But vibration induces only minor changes in du- ration and length of stance and swing phase, and on speed of walking and kinematics of lower limb segments. This paucity of effects is at variance with the perception of the subjects, who report illusion of leg stiffness and gait imbalance, as well as with the disturbing effects of vibration on qui- et stance. This speaks for a selective gating of Ia input during locomotion and emphasises the notion that the central nervous system can cope with an unusual continuous input along the Ia fibres from a key muscle like the soleus (120). It is responsible for the medium-latency response of the soleus to the stretch resulting from an unexpected perturbation during human walking (121). These findings support the hypothesis that, during walking the re- sponse to a perturbation of gait is not contributed to by velocity sensitive receptors, but by length-sensitive receptors (122), in keeping with the above described negligible effects of group Ia massive input. Load-related afferent feedbacks, in particular originating in Golgi tendon organ may al- so contribute to regulation of timing and intensity of muscle activity dur- ing walking (123). Descending control of dynamic equilibrium and body orientation Neural networks located in the spinal cord are capable of generating the basic motor pattern for locomotion. Nevertheless, the complexity of body balance maintenance requires descending modulation of spinal op- erations in order to coordinate movements of the two legs and the trunk. Furthermore, converging evidences indicate that implementation of spa- tially-oriented locomotor movements relies on head-centred internal ref- erences. It has been shown that if the head is horizontally turned or the eyes are laterally rotated, vibration of dorsal neck muscles during step- ping-in-place causes stepping in the direction of the naso-occipital axis or of the gaze, respectively (124). The walk trajectory deviates, or the body rotates during step- ping, to the side opposite to the vibrated muscle (50, 105, 125). Effects of unilateral vibration of and equilibrium control during sternomastoid muscle during stepping-in-place locomotion.

Uniodinated and iodinated a-fetoprotein were focused for 24 hours in a pH gradient 3 discount 40 mg aristocort overnight delivery. These curves also allow estimates of the specific activities which are listed in Table I cheap aristocort 4mg otc. Stability and physical properties of labelled ligands Labelled proteins prepared by the Iodogen method maintained high binding percentage for as long as about 8—10 weeks best buy aristocort. To examine the stability of the labelled proteins buy 40 mg aristocort overnight delivery, several labelled antigens were re-chromatographed on gel filtration columns after various periods of storage. It is important that the integrity of the protein molecule is preserved after labelling. The ideal method for radiolabelling of antigens for radioimmunoassays should be easy, inexpensive, and reproducible, yielding labelled ligands with high specific activity, high immunoreactivity, purity and long shelf-life. Since the Iodogen method seemed to approach these criteria, we have studied the reaction conditions and the application of this labelling method in our radioimmunoassays for proteins and polypeptides. For practical reasons we prefer polyethylene tubes with screw caps, even if the iodination is equally efficient when carried out in glass tubes. Since maximum incorporation is obtained after 7—13 min, we have routinely used a reaction time of 10 min. The apparent decrease in incorporation after 15—30 min could possibly be due to the formation of aggregates unable to enter the gel filtration column. However, the disappearance of radioactivity at pH 5, presumably as hydrogen iodide, suggests that pH below 6 should be avoided. A molar ratio of Iodogen to protein of 8 is sufficient for maximum incorpora­ tion. As each Iodogen molecule contains four chlorine atoms, this implies a 32:1 molar ratio of chlorine to protein. Besides,the sample is not mixed with the oxidizing agent in solution which means that molecules are not directly subjected to oxidation. The identical behaviour of labelled and unlabelled antigen when subjected to isoelectric focusing seems to exclude the possibility of major conformational changes. The minor radioactive peak in the isoelectric focusing experiment might be labelled protein with changed isoelectric point. However, dissociation of I25I loosely bound to protein and successive association to some ampholines cannot be excluded. The parallelism of the self-displacement curves and standard curves in addition to the high percentage of labelled antigen bound in the presence of antibody excess suggest retained immunological activity. Their lack of success with Iodogen might be explained by the enormous molar excess of Iodogen and radioactive iodide used. That extensive damage occurred in their experiment is indicated by the structural alterations reported. Our experience strongly supports the view [6, 7] that Iodogen provides an effective, gentle, and simple way to iodinate proteins and polypeptides. Purification by immunoadsorbtion and comparison of the “A” and “B” forms of the enzymes, Biochim. One speaker reported poor results with iodination times of 20-60 s at room temperature. Another speaker reported more successful results with iodination times of 20-30 min at room temperature. It appeared that while the method was successful with certain protein and glycoprotein hormones, it was not effective for prolactin. It was noted that Ms Paus and her colleagues employed iodination times of 10 min at 0°C. A speaker pointed out that the Chloramine-T method had been successfully applied at low temperature to label unstable proteins, with the additional advantage that the resulting slower reaction was easier to control. In response to questions, Ms Paus indicated that the shelf-life of the Iodogen- coated tubes was longer when they were closed under nitrogen instead of air. Pipetting of the solution of Iodogen in methylene chloride was easy if performed quickly. A study was made regarding the reduction of total error in radioimmunoassays due to the use of a volume marker. Counting errors were higher because of the presence of the second isotope, but the total error was greatly reduced owing to a much lower experimental error. In addition, the speed of the separation step was increased as the operating procedure was greatly simplified. Many sophisticated analyses have been made of the statistical background of the computation of radioimmunoassay standard curves, but lessattention has been paid to methodological considerations. Because the separation phase is the major source of operator error [1] we have examined the benefit of the use of a second isotope as a volume marker. For this purpose we choose 22Na, which satisfies all criteria of a volume marker (minimal overlap with the spectrum of 125I, suitable shelf-life, even distribution in the soluble phase) [2 ]. Determinations on 100 samples of patients for which gastrine determinations were requested, were performed in duplicate. The separation of bound and free antigen was obtained by adding 20 mg charcoal suspended in 0. After centrifugation exactly 1 mL of the supernate was pipetted into a tube and the rest of the supernate was pipetted into a separate tube. All counts were corrected for channel overlap and background to net counts for I and Na in the 1 ml supernate (lsi and Nasi), the rest of the supernate (Ig2 and Nas¡) and the precipitate (lp and Nap ). Using all data or only part of them, four calculation methods corresponding to different experimental procedures were used : 1 - counting of free and bound antigen without volume corree tion. A - counting of 1 mL supernate with an average total activity and with an average volume correction factor. The standard curves and values for the unknowns were obtained using the polygonal interpolation method [3]. The variance of the total error on the percent bound (varx), which can be considered as the sum of the counting error and the experimental error, was obtained from the variance o£ the differences between duplicates (vard): varx = vard/2. To derive the counting error we used the Gauss theorem for the variance of a variable which is a function of other variables. Table I summarizes variances for total error, experimental error and counting error for the four calculation methods under consideration, i. It will be seen that the use of 22Na as a volume marker (methods 3 and 4) reduced the total error (P<0. When both fractions are counted, as in our routine procedure, the totals of iodium and sodium counts can be used as a check on operator performance and anomalies in these values signal meaningless results. This could be expected as for each sample two tubes are counted, and in each tube spillover and background substraction must be taken into consideration. As a compromise one could use method 4, which saves counting time , but has still the advantage of a simplified separation step. However, values of percent bound were systematically higher in methods using volume correction. This is due to the fact that after centrifugation the charcoal used for separation of bound and free antigen, traps a small amount of assay buffer and of bound antigen. Therefore, if results are used for extensive mathematical analysis such as the determination of the affinity constant, volume correction should preferably be used as results so obtained are more exact. Peeters stated that while he and his colleagues had been using the method for several years, they had yet to evaluate it statistically, both as regards assay errors and as regards errors in the calculation of affinity constants. A method is described for directly determining the composition of mixtures of cross- reacting substances. The method is simple and could easily be automated and extended to deal with systems containing more than two analytes. The most usual way to compensate for the effect of cross-reaction in an assay system is to separate potential cross-reactants, usually by a physico-chemical method or introduce a chemical modification step before assay. An alternative is to measure the cross-reactants directly in the biological sample without prior separation. In the absence of highly specific anti sera, the approach taken has been to construct graphical representations that describe the behaviour of mixtures of cross-reactants.

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Following transduction buy generic aristocort canada, it is proposed to enrich for gene-engineered cells by selection for the Neo gene by growth in G418-containing medium order aristocort cheap. Large numbers of transduced and culture expanded cells are proposed to be returned to the patient order generic aristocort line. The clinical protocols can be divided into three categories: (i) gene marking studies order aristocort amex, (ii) immunotherapy, and (iii) inhibi- tion of virus replication. Enhanced Immunity Hadida F, DeMaeyer E, Cremer I,Autran B, Baggiolini M, Debre P,Viellard V. Therapeutic reconstitution of human viral immunity by adoptive transfer of cytotoxic T lymphocyte clones. Intracellular immunization of human T cells with a hairpin ribozyme against human immunodeficiency virus type 1. The complex pathology of systemic joint destruction, which is still not completely understood, limits the generation of effective therapies. To date, most pharmacological approaches focus on interfering with pain and inflammation. Drug discovery efforts resulting in useful agents have come into rheumatology empirically rather than through specific design. However, none of the drugs used today to ameliorate the pain and suffering of arthritis clearly prevents the progressive destruction of joints. Recently, there has been enormous progress in elucidating the molecular and cel- lular basis of rheumatoid joint destruction. Based on these data, novel strategies to inhibit rheumatoid joint destruction have been proposed and developed. There is great potential in the technology of gene therapy for specifically modifying disease mechanisms in the context of the aggressive behav- ior of cells resulting in the rheumatoid joint destruction. However, gene transfer methods can be used as a general vehicle for the delivery of a variety of gene products, thereby increasing the scope of diseases for which gene therapy can be used, such as for acquired diseases. Apart from the problem of how to correct a specific genetic abnormality or deliver a certain gene construct, the question of which path- ogenic pathway to modulate becomes crucial. However, the pro- gressive destruction of joint cartilage and bone represents a unique and most promi- nent feature of this disease. They are characterized by a large, more round shape than normal synovial fibroblasts, and have large pale nuclei with prominent nucleoli. These changes, together with some alterations in their behavior, suggest these cells to be “trans- formed-appearing” fibroblasts. Although these cells are activated, they do not reveal an increased rate of proliferation. Such events mirror the transformation events that occur in carcinogenesis (see Chapter 11). Apoptosis may alter the synovial lining layer that mediated the progressive destruc- tion of cartilage and bone. Less than 1% of lining cells exhibit morphological fea- tures of apoptosis as determined by ultrastructural methods, and several studies have reported the expression of antiapoptotic molecules such as bcl-2 and sentrin in synovial cells. This dysbalance may lead to an extended life span of synovial lining cells as well as result in a prolonged expression of matrix-degrading enzymes at sites of joint destruction. Activation of synovial cells results in the up- regulation of these adhesion molecules. But, conversely, the expression of early cell cycle genes such as c-fos and c-myc is stimulated further by cell adhesion molecules. Thus, the cellular interactions of neighboring macrophage-like cells, fibroblasts, and also chondrocytes appear to contribute to the perpetuation of chronic synovitis. However, the utilization of viral vectors for gene transfer requires substan- tial changes to the original viral genome. Apart from introducing the desired gene, these changes include modifications that disable replication of viral particles in infected cells. Transfection of packaging cells, which produce the virus envelope, results in the production of repli- cation-deficient virus particles. This would avoid multiple surgical interventions, which is a major disadvantage of ex vivo approaches. Another limiting factor, however, is the unpredictable site of insertion into the host genome resulting in, at least, a poten- tial risk of insertional mutagenesis. These models have provided important insights into mole- cular mechanisms of joint inflammation and helped elucidate key aspects of joint destruction. Therefore, these models have been used to study the effect of gene transfer approaches. However, with respect to the perichondrocytic cartilage degradation, there was a clear effect. Only few implants showed a slight reduction of invasiveness by synovial fibroblasts, which failed to reach statistical significance. Therefore, it has been speculated that this increase reflects an insufficient inhibitory response of the activated immune system in the synovium. Currently, studies are being performed investigating the feasibility of this approach as well as the delivery of further cytokine genes. One mechanism to block signaling pathways is the utilization of dominant negative mutants of signaling molecules such as c-Raf. Dominant negative (dn) mutants represent mutated variants of these molecules, which lack function. All steps were performed under strict safety condition including the screening for replication-competent retroviruses. The preliminary results of this study indicate that genes can be delivered to human joints safely and effectively. The final evaluation of the removed joints will be performed and include conven- tional histological evaluation as well as in situ hybridization and immunohisto- chemistry techniques. Novel strategies to inhibit rheumatoid joint destruction have been pro- posed and developed. There is great potential in the technology of gene therapy for specifically modifying disease mechanisms in the context of the aggressive behavior of cells resulting in rheumatoid joint destruction. Interfering with the stimulation of synovial cells by cytokines and growth factors 2. Direct inhibition of matrix-degrading enzymes such as matrix metallopro- teinases and cathepsins. Clinical trial to assess the safety, feasibility, and efficacy of transferring a potentially anti-arthritic cytokine gene to human joints with rheumatoid arthritis. Somatic mutations in the p53 tumor suppressor gene in rheumatoid arthritis synovium. Tomita T, Takeuchi E, Tomita N, Morishita R, Kaneko M, Yamamoto K, Nakase T, Seki H, Kato K, Kaneda Y, Ochi T. Suppressed severity of collagen-induced arthritis by in vivo transfection of nuclear factor kappaB decoy oligonucleotides as agene therapy. Federally supported research is regulated by the federal gov- ernment in the context of animal care and their humane use, as well as for the safe and ethical use of humans in clinical trials. A brief historical account of federal regulation is presented along with current regulatory requirements as well as potential future changes in review and approval procedures. Already, sheep, cows, and primates have been cloned using nuclear transfer techniques (see Chapter 2). At that time, using the nuclei of tadpoles transferred into frog eggs, scientists raised cloned tadpoles and even adult frogs. Recent embryonic cloning work was published in 1996 when lambs were reported cloned from embryos. In the case of Dolly, modifications in the previously successful protocols resulted in the ability to clone using an adult cell, a mammary cell reprogrammed to “dedifferentiate,” and thus permitting the development of an adult animal. In March, 1997, scientist in the United States announced the cloning of primates from embryonic cells using nuclear transfer. These techniques have an obvious extension of cloning humans, and that has startled the research and lay communities alike.

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