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However purchase 60caps mentat overnight delivery medicine 20th century, progress in treatment may ality disorder or impulsive traits buy mentat 60caps with visa medicine xyzal, appears to be associated be reflected in improved cognitive function (263) cheap mentat 60caps otc symptoms pregnancy. Consis- with behavioral discount mentat 60caps treatment 1st line, physiologic, and structural evidence of PFC tent with the view that treatment may modulate cognitive dysfunction. An important and unanswered question is, recovery, some cognitive deficits in recovering patients ap- How does PFC dysfunction contribute to the vulnerability pear to respond to cognitive rehabilitation (264). Hypotheses have been presented that suggest In summary, the behavioral studies describe the display that alcoholism is just one of several forms of impulsive of deficits in cognitive functions that may have implications behavior that these individuals fail to inhibit due to a general for circuitry dysfunction in alcoholism: executive function deficiency in behavioral inhibition or as a consequence of deficits associated with the prefrontal cortex, visual-spatial the failure to anticipate the negative consequences of alco- deficits associated with the parietal cortex, and learning/ holism (269,270). Overall, these studies reward dysfunction hypothesis resting on a consideration of are consistent with the findings related to reduced tissue the impact of PFC dysfunction on mechanisms underlying volume on MRI, reductions in cortical metabolism with reward. The PFC input into limbic structures responsible fluorodeoxyglucose (FDG)-PET (242), and information for reward is critical to the experience, anticipation, and processing deficits in ERP studies (265). The activation of PFC outputs plies a connection between alterations in brain structure, to limbic structure causes a release of glutamate that may function, and behavior related to alcoholism. From this perspective, PFC activation serves THE INTERPLAY OF THE NEURAL as a 'brake' on reward mechanisms. In fact, it is tempting CIRCUITRY AND NEUROCHEMISTRY OF to think of this PFC-NAc interplay as a pathway contribut- ALCOHOLISM: IMPLICATIONS FOR ing to the capacity of human judgment to restrain impulsive TREATMENT reward-related behavior. Yet abnormal PFC input would also be expected to disturb NAc function with respect to Ethanol has multiple specific effects on amino acid, mono- both the processing of rewarding stimuli generally and drugs amine, and neuropeptide neurotransmitter systems, and of abuse in particular. Thus, it may not be surprising that 1436 Neuropsychopharmacology: The Fifth Generation of Progress the familial vulnerability to alcoholism is associated with ality disorder and alcohol-induced aggression. Alcohol Clin Exp both PFC functional deficits and alterations in the capacity Res 1998;22:1898–1902. Effect of drugs and alcohol on psychomotor skills of drugs representing multiple component actions of related to driving. Complications of alco- aversive experiences in humans. If so, then genes controlling hol withdrawal: pathophysiological insights. Alcohol Health Res corticolimbic neurodevelopment and genes encoding the World 1998;22:61–66. Symptomatology in alcoholics at various stages of abstinence. Alcohol Clin Exp tion may provide a diversity of potential foci for the study Res 1985;9:505–512. The Wernicke-Korsakoff The cellular adaptations to chronic ethanol underlie tol- syndrome and related neurologic disorders due to alcoholism and erance to ethanol effects and withdrawal symptoms that malnutrition. Anaesthetics set their ment of glutamatergic function and a deficit in GABAergic sites on ion channels [news; comment]. When examined beyond these generalizations, the 334–335. Sites of alcohol and volatile For example, dependence-related adaptations may be re- anaesthetic action on GABA (A) and glycine receptors [see com- ments]. Receptor andion channel nomen- or perhaps changes in receptor subunit composition. Trends Pharmacol Sci 1996;17: a critical juncture in the treatment of alcoholism because 348–355. Cellular and behavioral neurobiology risk, motivate relapse to ethanol use, induce withdrawal- of alcohol: receptor-mediated neuronal processes. Clin Neurosci related neuroplasticity that can increase risk for subsequent 1995;3:155–164. Factors that enhance ethanol inhibition of N-methyl-D-aspartate receptors in cerebellar gran- mote neurotoxicity. In light of these issues, novel treatments ule cells. Developmental decrease in ethanol inhibition of N-methyl-D-aspartate receptors in rat neocortical neurons: ACKNOWLEDGMENTS relation to the actions of ifenprodil. This work was supported by the National Institute on Alco- 19. Ethanol inhibits glutamate- induced currents in heteromeric NMDA receptor subtypes. Ethanol inhibits NMDA of Veterans Affairs (Alcohol Research Center, Clinical Neu- receptor-mediated excitotoxicity in rat primary neuronal cul- rosciences Division, National Center for Posttraumatic tures. Preferential stimulation of dopamine release in the nucleus accumbens of freely moving rats by ski for her assistance in preparing this manuscript. Biphasic effect of ethanol on extra- cellular accumulation of glutamate in the hippocampus and the nucleus accumbens. Ascending and descending rates of dent modulation of CA1 local circuit inhibition. J Neurosci change in blood alcohol concentrations and subjective intoxica- 1996;16:2034–2043.

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This portion of the search was not included in the final search update on August 1 best 60 caps mentat treatment ear infection, 2012 buy 60caps mentat with mastercard treatment research institute. The results from this search are reflected in the totals depicted in the literature flow diagram purchase mentat 60 caps with mastercard medications migraine headaches. Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab purchase 60 caps mentat overnight delivery treatment broken toe,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 MeSH descriptor Prognosis explode all trees OR MeSH descriptor Sensitivity and Specificity explode all trees OR MeSH descriptor Treatment Outcome explode all trees OR MeSH descriptor Diagnosis explode all trees OR predictors:ab,ti OR predict:ab,ti OR predicting:ab,ti OR predicts:ab,ti OR predicted:ab,ti OR prognosis:ab,ti OR prognostic:ab,ti OR accurately:ab,ti OR accuracy:ab,ti OR accurate:ab,ti OR reliability:ab,ti OR sensitivity:ab,ti OR specificity:ab,ti OR diagnostic:ab,ti #3 maintain:ab,ti OR maintenance:ab,ti OR maintained:ab,ti OR success:ab,ti OR successful:ab,ti OR conversion:ab,ti OR restoration:ab,ti OR restored:ab,ti A-12 #4 #1 AND #2 and #3 #5 #4, Limits: Cochrane Reviews, 2000-2011 Grey Literature Searches ClinicalTrials. Data Abstraction Elements Study Characteristics • Study Identifiers o Study Name or Acronym o Last name of first author o Publication Year • Additional Articles Used in This Abstraction • Study Objectives • Study Dates o Enrollment Start (Mon and YYYY) o Enrollment End (Mon and YYYY) o Follow-up End (Mon and YYYY) • Study Sites o Single Center, Multicenter, Unclear/Not reported, Other (specify) o Number of sites • Geographic Location (Select all that apply) o US, Canada, UK, Europe, S. America, Asia, Africa, Australia/NZ, Unclear/Not reported, Other (specify) • Study Design o Prospective RCT o Prospective cohort o Retrospective cohort o Case-control o Cross-sectional o Other (specify) • Funding Source (Select all that apply) o Government, Industry, Non-govt/Non-industry, Unclear/Not reported, Other (specify) • Setting (Select all that apply) o In-patient, Out-patient, Emergency Room, Unclear/Not reported, Other (specify) • Enrollment Approach (Select all that apply) o Consecutive patients, Convenience sample, Unclear/Not reported, Other (specify) • Study Inclusion and Exclusion Criteria o Copy/paste inclusion and exclusion criteria as reported o Is the study entirely composed of patients with any of the following characteristics/ conditions? Record the following elements for Total Population, Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) • Number of Patients, Age, Ethnicity, and Race o Number of Patients  Total  Female  Male o Percentage  Female  Male o Age  Mean  Standard Deviation  Standard Error  Median  IQR  Min  Max  NR o Ethnicity  Hispanic or Latino  Not Hispanic or Latino  NR o Race  Black/African American  American Indian or Alaska Native  Asian  Native Hawaiian or other Pacific Islander B-2  White  Multiracial  Other (specify)  NR • Co-morbidities and Previous Treatment Failures o Diabetes  N  % o Heart failure, All types (define)  N  % o Heart failure, Systolic (define)  N  % o Heart failure, Diastolic (define)  N  % o Hypertension  N  % o Kidney disease (define)  N  % o Hypertrophic cardiomyopathy (define)  N  % o Thyroid disease (define)  N  % o Pulmonary disease (define)  N  % o Coronary artery disease  N  % o Enlarged left atrium (define)  N  % o LVEF, Mean or median  Mean  Median  SD  SE  IQR o LVEF, Number of patients (<35% or other [define])  N B-3  % o Previously failed rate-control pharmacological therapy (define)  N  % o Previously failed rhythm-control pharmacological therapy (define)  N  % o Duration of AF (include units)  mean  Median  SD  SE  IQR o Permanent AF  N  % o Paroxysmal AF  N  % o Persistent AF  N  % • Comments Intervention Characteristics. Record the following elements for Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) • Intervention Characteristics o Intervention Components (check all that apply)  Placebo or control  Pharmacological agents for rate control  Procedures for rate control  Pharmacological agents for rhythm control  Procedures for rhythm control o Placebo/Control Details  Placebo  Usual care control/optimal medical therapy  Other (specify) o Rate-control Pharmacological Agent Details  Beta-blockers • Acebutolol • Atenolol • Bisoprolol • Carvedilol • Esmolol • Metoprolol • Nadalol B-4 • Nebivolol • Timolol • Specific medication not reported  Calcium channel blockers • Diltiazem • Verapamil • Specific medication not reported • Other o Amiodarone o Digoxin o Dronedarone o Specific medication not reported o Rate-control Procedure Details  AVN ablation and permanent pacemaker implantation o Rate-control Target  Strict (define)  Lenient (define)  Other (define)  NA o Rhythm-control Pharmacological Agent Details  Amiodarone  Beta-blockers • Acebutolol • Atenolol • Carvedilol • Esmolol • Metoprolol • Nadalol • Nebivolol • Timolol • Specific medication not reported  Calcium channel blockers • Diltiazem • Verapamil • Specific medication not reported  Disopyramide  Dofetilide  Dronedarone  Flecainide  Ibutilide  Propafenone  Sotalol o Rhythm-control Procedure Details  Electrical cardioversion  Pulmonary vein ablation – open surgical B-5  Pulmonary vein ablation – minimally invasive  Pulmonary vein ablation – transcatheter  Surgical Maze  Cardiac resynchronization • Intervention Descriptors o Describe the intervention received by patients in Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) • Duration of Follow-up - Record the following elements for Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) o Mean follow-up o Mean Variability (SD, SE, IQR) o Median follow-up o Median Variability (SD, SE, IQR) • Comments Outcomes • Select the outcome reported on this form o Restoration of sinus rhythm (conversion) o Maintenance of sinus rhythm o Recurrence of AF (specify time period) o Development of cardiomyopathy o All-cause mortality o Cardiac mortality o Myocardial infarction o CV hospitalizations o AF Hospitalizations o Heart failure symptoms o Control of AF symptoms (e. B-11 • Overall Study Rating (Good/Fair/Poor) o Good (low risk of bias). These studies have the least bias, and the results are considered valid. These studies adhere to the commonly held concepts of high quality, including the following: a clear description of the population, setting, approaches, and comparison groups; appropriate measurement of outcomes; appropriate statistical and analytical methods and reporting; no reporting errors; a low dropout rate; and clear reporting of dropouts. These studies are susceptible to some bias, but not enough to invalidate the results. They do not meet all the criteria required for a rating of good quality because they have some deficiencies, but no flaw is likely to cause major bias. The study may be missing information, making it difficult to assess limitations and potential problems. These studies have significant flaws that may have invalidated the results. They have serious errors in design, analysis, or reporting; large amounts of missing information; or discrepancies in reporting. Use the PICOS format to identify specific issues, if any, that may limit the applicability of the study to this review. List of Included Studies Abreu Filho CA, Lisboa LA, Dallan LA, et al. Effectiveness of the maze procedure using cooled- tip radiofrequency ablation in patients with permanent atrial fibrillation and rheumatic mitral valve disease. Combined radiofrequency modified maze and mitral valve procedure through a port access approach: early and mid-term results. Prospective, randomized comparison of two biphasic waveforms for the efficacy and safety of transthoracic biphasic cardioversion of atrial fibrillation. Randomized study of surgical isolation of the pulmonary veins for correction of permanent atrial fibrillation associated with mitral valve disease. Randomised comparison of antero-lateral versus antero- posterior paddle positions for DC cardioversion of persistent atrial fibrillation. A randomized controlled trial of efficacy and ST change following use of the Welch-Allyn MRL PIC biphasic waveform versus damped sine monophasic waveform for external DC cardioversion. Maintenance of sinus rhythm in patients with atrial fibrillation: an AFFIRM substudy of the first antiarrhythmic drug. Small or large isolation areas around the pulmonary veins for the treatment of atrial fibrillation? Exercise capacity in atrial fibrillation: a substudy of the Sotalol-Amiodarone Atrial Fibrillation Efficacy Trial (SAFE-T). Pharmacological conversion of recent atrial fibrillation: a randomized, placebo-controlled study of three antiarrhythmic drugs. Thyroid function abnormalities during amiodarone therapy for persistent atrial fibrillation. Long-term efficacy and safety of propafenone and sotalol for the maintenance of sinus rhythm after conversion of recurrent symptomatic atrial fibrillation. Success of serial external electrical cardioversion of persistent atrial fibrillation in maintaining sinus rhythm; a randomized study. Randomized study comparing duty-cycled bipolar and unipolar radiofrequency with point-by-point ablation in pulmonary vein isolation. Blomstrom-Lundqvist C, Johansson B, Berglin E, et al. A randomized double-blind study of epicardial left atrial cryoablation for permanent atrial fibrillation in patients undergoing mitral valve surgery: the SWEDish Multicentre Atrial Fibrillation study (SWEDMAF). Atrial Fibrillation Catheter Ablation Versus Surgical Ablation Treatment (FAST): A 2-Center Randomized Clinical Trial. DC cardioversion of persistent atrial fibrillation: a comparison of two protocols. Higher energy monophasic DC cardioversion for persistent atrial fibrillation: is it time to start at 360 joules?. Anterior-posterior versus anterior-lateral electrode position for biphasic cardioversion of atrial fibrillation.

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The comparatively high recent this finding is presented in Table 67 purchase mentat 60caps with mastercard medicine bg. These results are survey indicates that the combined effects of these three based on synthetic cohort analyses using retrospective age- components are strong buy mentat 60 caps without prescription symptoms thyroid cancer. This is true discount 60 caps mentat amex treatment emergent adverse event, in part mentat 60caps line medicine kit for babies, because anxiety at-onset reports to evaluate intercohort differences in life- and stress disorders occur to a high proportion of the popu­ time risk of anxiety disorders over a period of four decades. It is also true The data are clear in showing that the relative odds of having because these disorders have comparatively early ages at an anxiety disorder have steadily increased over this period onset and high rates of chronicity. More detailed analyses of these and other data show that Retrospective reports about age at onset are routinely the increased prevalences of anxiety disorders are more pro­ collected in epidemiologic surveys and used to estimate syn­ nounced than the increased prevalences of other mental dis­ thetic onset distributions. Furthermore, the increasing prevalences within the is less than 15 years of age. The only commonly occurring anxiety disorders have been found to be especially pro­ chronic physical disorder that has a similar age-at-onset dis­ nounced for GAD, generalized social phobia, and PTSD. All other commonly occurring chronic physical disorders that have been shown to have an effect on role functioning have median ages at onset that occur much later, in some cases decades later, than anxiety disorders. Other mental disorders, including depression, TABLE 67. THE EFFECTS (ODDS RATIOS) OF substance use disorders, oppositional-defiant disorder, con- COHORT IN PREDICTING LIFETIME ANXIETY DISORDERS IN SIX COUNTRIESa duct disorder, and attention-deficit hyperactivity disorder, also have comparatively early ages at onset, although anxiety Age Group disorders are the temporally primary disorders in the vast 2 majority of people with a lifetime history of any mental 18–24 25–34 35–44 45–54 χ 3 disorder (34). No information is available, in comparison, Brazil 3. Although psychiatric epidemiologic surveys typically are From WHO International Consortium of Psychiatric Epidemiology: cross-national comparisons of the prevalences and correlates of cross-sectional, making it impossible to track illness course, mental disorders: an ICPE study. Bull WHO 2000;78:420, with indirect assessments of chronicity in these surveys have been permission. Age-at-onset distributions for any anxiety disorders in six countries. Cross-national comparisons of the prevalences and correlates of mental disorders: an ICPE study. The question implicitly addressed by specific lifetime mental disorders. Results clearly suggest these studies is whether it is in the financial interests of that anxiety disorders are the most chronic of all mental employers to invest in employee health care. This indirect evidence is consistent with the increased direct costs of treatment be offset by decreased results of longitudinal studies carried out in clinical samples, indirect costs in such things as sickness absence, poor work which uniformly show that anxiety disorders are typically performance, and accidents? This important question is dis­ very chronic (36–38). It is noteworthy that this high chron­ cussed below. However, even when the focus is on narrow icity is not greater than that found among a number of financial costs, the preceding is not the only question of impairing physical disorders, such as arthritis, asthma, and importance in evaluating the societal costs of illness. However, the combined occurrence of high life- Equally, if not more, important from a societal perspective time prevalence with early age at onset and high chronicity is the question of whether the human capital potential of makes anxiety disorders unique. The one chronic physical the individual is adversely affected by illness. Specifically, disorder with comparable lifetime prevalence and early what difference does the existence of a particular chronic onset, hay fever, is active for only a few weeks each year. Epidemiologic data also show that anxi­ ADVERSE EFFECTS ON SECONDARY ety is associated with elevated risk of subsequent unemploy­ OUTCOMES ment (42,43). Clinical experience also suggests that anxiety is associated Virtually all cost-of-illness studies focus on the effects of with more subtle decrements in role performance. It is com­ prevalent disorders on current role functioning, taking cur- mon for patients with chronic GAD or PTSD, for example, 986 Neuropsychopharmacology: The Fifth Generation of Progress to work at low-paying jobs because they are unable to cope of a day or working less efficiently than usual) during the with the stresses of higher paying jobs. This would be con­ month prior to the interview (51). Each of the six anxiety sidered a cost of illness from the societal perspective, but not disorders evaluated in that study (GAD, panic disorder, spe­ from the perspective of the employer. Very little scientific cific phobia, social phobia, agoraphobia, and PTSD) had evidence exists regarding opportunity costs of this sort. The significant effects on work-cutback days, from a high of most sustained examination of these costs was carried out 4. None of the six was signifi­ (NCS) in which retrospective reports about the ages at onset cantly associated with work-loss days, implying that anxiety of individual mental disorders were used to define time- influences work largely by affecting the quality of perfor­ varying predictors of subsequent transitions in educational mance on days at work rather than by reducing the amount attainment (44), teen childbearing (45), marital timing and of time spent at work. The results clearly show The MIDUS survey yielded information that is even that mental disorders, in general, and anxiety disorders, in more interesting because it assessed both mental and physi­ particular, are associated with significantly elevated risks of cal disorders. Gross bivariate analyses showed that two men­ several different life course events that have important ad- tal disorders, both anxiety disorders, were among the top verse financial implications. In terms of standardized (for five of all chronic conditions in terms of average per capita sociodemographics) odds ratios, NCS respondents with number of past month work impairment days. These top some early-onset anxiety disorders had 40% elevated odds five included GAD (6. Further- ity, and 150% elevated odds of current unemployment at more, multivariate analyses controlling for age, gender, and the time of interview.

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C purchase 60caps mentat overnight delivery treatment xeroderma pigmentosum, Typical Antibody deposition presentation and pathologic features buy 60caps mentat visa medicine hollywood undead. Chronic Oxidized LDL rejection occurs during a span of m onths Typical clinical presentation Infection Gradual increase in creatinine (months) to years order mentat 60 caps with visa medications dispensed in original container. It appears to be unresponsive to Non-nephrotic–range proteinuria current treatm ent and has em erged as the T cells m ajor problem facing transplantation buy 60 caps mentat otc medicine 6 year in us. No recent nephrotoxic events M acrophages Because chronic rejection is thought to be the Key pathologic features Platelet aggregates end result of uncontrolled repetitive acute Interstitial fibrosis rejection episodes or a slowly progressive Arterial fibrosis and intimal thickening inflam m atory process, its onset m ay be as Cytokines/ early as the first few weeks after transplan- growth factors tation or any tim e thereafter. D, The likely sequence of events in chronic Cell proliferation rejection and potential m ediating factors for Fibrosis key steps. Progressive azotem ia, proteinuria, and hypertension are the clinical hallmarks Tubulointerstitial of chronic rejection. Im m unologic and Vascular injury injury nonimmunologic mechanisms are thought Arteriosclerosis Glomerular sclerosis to play a role in the pathogenesis of this entity. Im m unologic m echanism s include antibody-m ediated tissue destruction that Reduced nephron occurs possibly secondary to antibody- mass dependent cellular cytotoxicity leading to obliterative arteritis, growth factors derived from m acrophages and platelets leading to Graft loss D fibrotic degeneration, and glomerular hyper- tension with hyperfiltration injury due to reduced nephron mass leading to progressive glomerular sclerosis. Nonimmunologic causes can also contribute to the decline in renal function. Atheromatous renovascular disease of the transplant kidney m ay also be responsible for a significant num ber of cases of progressive graft failure. ATG— antithym ocyte globulin; ATN — acute tubular necrosis; BP— Slowly rising creatinine blood pressure; CsA— cyclosporine; LDL— low-density lipoprotein. Check CsA level High Low Lower CsA dose and repeat creatinine Improved No improvement Ultrasound Obstruction No obstruction Biopsy Rejection ATN Glomerulonephritis Recurrent GN de novo GN Acute Acute Chronic on chronic Adjust immunosuppressant Temporizing measures Steroid bolus Control BP OKT3 or ATG Avoid nephrotoxins E FIGURE 9-7 BANFF CLASSIFICATION OF RENAL The Banff classification of renal allograft rejection. This schem a is ALLOGRAFT REJECTION an internationally agreed on standardized classification of renal allograft pathology that regards intim al arteritis and tubulitis as the m ain lesions indicative of acute rejection. Normal Patchy mononuclear cell infiltrates without tubulitis is not uncommon Borderline changes No intimal arteritis; mild tubulitis and endocapillary glomerulitis Acute rejection Grade I: tubulitis ++ Grade II: tubulitis with glomerulitis Grade III: intimal arteritis, interstitial hemorrhage, fibrinoid, thrombosis Transplant Rejection and its Treatment 9. A 23- or 25-gauge spinal needle is used under aseptic conditions. A 20-mL syringe containing 5 mL of RPM I-1640 tissue culture medium is connected to the needle. Ultrasound guidance m ay be used on the rare occasions when the graft is not easily palpable. M onitoring of other products of inflam m ation such as neopterin Constant (but not excessive) suction and lym phokines continues to be explored. It has been shown that acute rejection is associated with elevated plasm a interleukin (IL)-1 in azathioprine-treated patients and IL-2 in cyclosporine-treated patients. IL-6 is also increased in the serum and urine im m ediately after transplantation and during acute rejection episodes. The m ajor 25-G needle problem, however, is that infection, particularly viral, can also elevate cytokine levels. Recently, polym erase chain reaction (PCR) has also Transplanted kidney been used to detect m RN A for IL-2 in fine-needle aspirate of hum an transplant kidney [7,8]. Using the PCR approach, IL-2 could be W ound detected 2 days before rejection was apparent by histologic or clinical Inguinal ligament criteria. Reverse transcriptase–PCR has also been used to identify intrarenal expression of cytotoxic molecules (granzyme B and perforin) and im m unoregulatory cytokines (IL-2, -4, -10, interferon gam m a, and transform ing growth factor-b1) in hum an renal allograft biopsy specim ens. M olecular analyses revealed that intragraft display of m RN A encoding granzym e B, IL-10, or IL-2 correlates with acute rejection, and intrarenal expression of transform ing growth factor (TGF)-b1 m RN A is associated with chronic rejection. These data suggest that therapeutic strategies directed at the m olecular correlates of rejection m ight refine existing antirejection regim ens. Treatment FIGURE 9-9 IM M UNOSUPPRESSION Im m unosuppressive therapy protocols. Standard im m unosuppressive therapy in renal PROTOCOLS transplant recipient consists of 1) baseline therapy to prevent rejection, and 2) short courses of antirejection therapy using high-dose m ethylprednisolone, m onoclonal antibodies or poly- clonal antisera such as antilym phocyte globulin (ALG) and antithym ocyte globulin (ATG). Induction protocols Antilymphocyte globulin is prepared by immunizing rabbits or horses with human lymphoid Maintenance protocols cells derived from the thym us or cultured B-cell lines. Disadvantages of using polyclonal Early posttransplantation ALS include lot-to-lot variability, cum bersom e production and purification, nonselective targeting of all lym phocytes, and the need to adm inister the m edication via central venous Late posttransplantation access. Despite these lim itations, ALG has been used both for prophylaxis against and for Antirejection therapy the prim ary treatm ent of acute rejection. A typical recom m ended dose for acute rejection is 10 to 15 m g/kg daily for 7 to 10 days. The reversal rate has been between 75% and 100% in different series. In contrast to m urine m onoclonal antibodies (eg, O KT3), ALS does not generally induce a host antibody response to the rabbit or horse serum.