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Generic medications often are available in lieu of brand-name drugs. The review team noted several examples in which an expensive brand-name medication was prescribed to foster children despite the ready availability of low-cost alternatives. For instance, Ortho Tri-Cyclen is a brand-name medication; in fiscal 2004, there were three low-cost generic alternatives to the drug, TriNessa, Tri-Sprintec and Tri-Previfem. TriNessa and Tri-Sprintec entered the market in December 2003 and Tri-Previfem became available in April 2004.3 Of 739 prescriptions for Ortho Tri-Cyclen written for Texas foster children in fiscal 2004, 258 were written and filled after the generic medications became available. These 258 prescriptions cost Texas taxpayers , 943.38. If the least expensive generic medication Tri-Sprintec ; had been prescribed instead, at about .69 per prescription, the state would have paid only , 144.02--, 799.36 or about 40 percent less Exhibit 29 ; . In most cases, prescribing a brand-name medication when a generic version is available is fiscally irresponsible.

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Pulmonary edema, anaphylaxis, asthma, COPD: 2.5mg by nebulizer Asthma: 1 year old 1.25mg by nebulizer 1 year old 2.25mg by nebulizer Tachydysrhythmias Tachydysrhythmias, anxiety, nausea and vomiting and infliximab.
1.6 Project Goals There is a lack of information in the scientific literature regarding the incidence, kinetics, residues and efficacy of IP antimicrobial use in cattle. A series of research projects were designed to provide the data necessary to answer these questions.

Membrane is unclear, and the existence of a hormonally regulated, labile protein which facilitates this transfer had been predicted for many years 1, 3 ; . The recently discovered steroidogenic acute regulatory protein StAR ; is a 30 mitochondrial protein which has many of the characteristics of this regulator 3, 4 ; . StAR has been demonstrated to promote movement of cholesterol from the outer to the inner mitochondrial membrane where P450-SCC catalyses the first, and rate limiting, enzymatic step in steroid synthesis 5, 6 ; . In addition, expression of StAR promotes steroidogenesis, and directly facilitates the transfer of cholesterol and other sterols in reconstituted mitochondria 7-9 ; . Perhaps the most convincing evidence that StAR is critical for this process in vivo is the observation by Miller and others that mutations in the StAR gene cause congenital lipoid adrenal hypoplasia 10, 11 ; . In this autosomal recessive disorder, gonadal and adrenal steroid production are blocked at the level of cholesterol side chain cleavage, resulting in a massive accumulation of cholesterol in the adrenal glands 10 ; . Likewise, mice in which the StAR gene is disrupted have a severe reduction in corticosterone synthesis and accumulate massive lipid deposits in their adrenal cortex 12 and intal. Both associated with increased severity of hepatic lesions. Women are at higher risk for fatty liver as are patients with decreased creatinine clearance. PIs can cause both hepatocellular and cholestatic disease; a pattern of ballooning degeneration with pericellular fibrosis is associated with administration of ritonovir. Combination therapy may cause even greater hepatoxicity. Indinavir and Atazanavir inhibit hepatic enzymes and can cause asymptomatic, reversible hyperbilirubinemia similar to Gilbert syndrome. Metabolic dysfunction and morphologic abnormalities Lipid and glucose abnormalities are also associated with mitochondrial dysfunction. Three forms of morphologic changes are seen in patients on antiretroviral therapy: lipodystrophy, lipoatrophy, and lipohypertrophy. In lipodystropy fat accumulation is usually truncal with buffalo hump between the shoulders or increased abdominal girth, but has also manifested as gynecomastia and multiple lipomas. Lipoatrophy is peripheral and includes diffuse or focal fat loss in the limbs or the face. Patients with lipodystrophy were more likely to have truncal adiposity, impaired glucose tolerance, diabetes, hypertriglycerides and decreased HDL. Cardiovascular disease risk factors are markedly elevated in patients with fat redistribution. Breast lipodystrophy and gynecomastia increased in men on HAART. Cardiovascular disease can be a result of lipid and glucose abnormalities or from toxic effects of lactic acid. Myocyte necrosis, cardiomyopathy and arteriosclerosis all contribute in the cardiovascular disease in this population. Age, smoking history and genetic risk factors increase the rates of cardiovascular pathology. Early studies show dramatic increases in carotid artery intima-media thickness. This can be reversed with lipid-lowering agents. The true impact of HAART on coronary artery atherosclerosis and subsequent myocardial infarctions will probably increase with duration of therapy, especially in those with known cardiac risk factors of smoking and hypertension. Osteonecrosis and osteopenia Osteonecrosis with avascular necrosis is increased in patients on antiretroviral therapy. Suggested mechanisms include: antiphospholipid antibodies, hyperlipidemia PIs may contribute to lipid abnormalities, but are not the sole factor ; . Patients on tenofovir appear to have increased loss of bone mineral density. Hips and shoulders are the most common sites. It occurs in all known risk groups and is not associated with T-cell counts or viral load. Pain and radiologic evidence of fractures or lytic lesions may lead to request for a bone biopsy to rule out infection or malignancy. Histology reveals osteopenia, osteonecrosis with microsequelae, fibrosis, and osteoblastic activity. Immune Restoration Syndrome Following the initiation of highly active antiretroviral therapy HAART ; some patients develop exaggerated local and systemic inflammatory reactions. The immune restoration disease IRD ; , also known as immune restoration inflammatory syndrome IRIS ; usually occurs within the first 6 months of initiating therapy and coincides with a rapid increase in CD4 + Tlymphocytes and the resulting immune reconstitution. The reaction is thought to be due to increased hypersensitivity to the antigens. IRD reflects dysregulated immune responses against pre-existing infections with different immunopathological mechanisms for different pathogens.
A major task of the graduate school is the co-ordination and development of postgraduate education for the PhD participants, which is provided through the PE&RC educational programme. The objective of this programme is to enhance in-depth knowledge of PhD students on specific research issues, as well as broadening the students' scientific scope and integrating their own work in other research areas and improving communicative skills. These `T-shaped skills' broad scientific overview combined with in-depth knowledge of specific subjects ; allow for scientific, communicative and co-operative flexibility. This is crucial for a contemporary scientific career, since it is unlikely that the postdoctoral occupation will only be based on the specific work done during the PhD period. The educational programme includes postgraduate courses on various subjects such as statistics, modelling techniques, precision agriculture, crop protection and applied soil ecology ; , training modules, symposia, literature studies and PE&RC-PhD discussion groups. A Training and Supervision Plan TSP ; has been developed to assist PhD students in complying with PE&RC educational requirements. PhD students can only become a full member of the Graduate School when the TSP has been approved by the Educational Committee of the Graduate School. In essence, the plan is a guide for the educational activities associated with the PhD work, as well as an agreement on the type and frequency of supervision. As the TSP is officially signed by the candidate's supervisor, and approved by the Graduate School, it conveys certain rights and obligations. A candidate who has fulfilled the educational components stipulated in the TSP will receive a certificate from the Graduate School at the end of the public defence of the thesis and invirase.

Figure Legends Figure 1 Effects of ritonavir, nelfinavir and indinavir on electrical activity and voltagedependent K + currents. 10 M ritonavir A ; and 20 M nelfinavir B ; changed shape and frequency of glucose-induced action potenials, while 70 M indinavir C ; was without effect. Characteristic action potentials in the presence of the respective compounds are shown in the insets of Fig. 1 A, B, C at extended time scale. The experiments are representative of 5 with similar results for ritonavir, 6 for nelfinavir and 4 for indinavir. The terms 0.5G and 15G indicate a glucose concentration of 0.5 mM and 15 mM, respectively. 10 M ritonavir D ; and 20 M nelfinavir E ; partly inhibited the voltage-dependent K + current, 70 M indinavir was without effect F ; . The experiments are representative of 4 with similar results for ritonavir, 6 for nelfinavir and 7 for indinavir. Voltagedependent K + current was monitored every 15 s during 150 ms voltage-steps from -70 to 0 mV. Drugs were added as indicated by the horizontal bars and isdn.
GENERAL SYSTEMIC Antiretroviral therapy ; Combination antiretroviral ARV ; therapy is always recommended. Preferred regimens include two nucleoside reverse transcriptase inhibitors NRTIs ; along with either 1 or 2 protease inhibitors PIs ; or with the nonnucleoside reverse transcriptase inhibitor nNRTI ; efavirenz. Preferred NRTI combinations are zidovudine plus lamivudine or didanosine, and stavudine plus lamivudine or didanosine. Preferred PI therapy is with nelfinavir or indinavir, or with dual PI combination therapy with ritonavir plus indinavir, saquinavir, or lopinavir. Alternative NRTI combinations are didanosine plus lamivudine, and zidovudine plus zalcitabine. Alternative agents that can be used with 2 NRTIs include abacavir, amprenavir, delavirdine, nevirapine, ritonavir, saquinavir, and nelfinavir plus saquinavir. Cross-resistance among PIs is common, as is cross-resistance among nNRTIs. Zidovudine and stavudine should not be used in combination. Indinavir and saquinavir should not be used in combination. Other drug combinations might be necessary; resistance testing and expert consultation can be helpful. See text for further discussion Nucleoside reverse transcriptase inhibitors NRTIs ; Zidovudine AZT, Retrovir ; 200 mg po tid or 300 mg po bid; lower dosages eg, 100 mg 3 times daily ; for patients unable to tolerate higher dosages and patients with renal failure or cirrhosis. Available as liquid formulation. Available also as fixed-dose combinations: zidovudine 300 mg plus lamivudine 150 mg Combivir ; given as one tablet po bid; and zidovudine 300 mg plus lamivudine 150 mg plus abacavir 300 mg Trizivir ; , given as one tablet po bid. Take with or without food Didanosine ddI, Videx ; 400 mg po qhs as 2 200mg buffered tablets, or 200 mg po bid as 2 100-mg chewable tablets or 250mg po bid powder for patients 60 kg; 125 mg tablets ; or 167 mg powder ; po bid for patients 60 kg. Available as enteric-coated capsules Videx EC ; given as 400mg EC capsule po qd 60 250-mg EC capsule po qd 60 Dosage reduction ie, 200 mg d ; in renal failure. Take on an empty stomach Until efficacy wanes or toxicity occurs NRTI drug class effects: Nausea, vomiting; aminotransferase elevations alanine transaminase [ALT], aspartate transaminase [AST] lactic acidosis with hepatic steatosis; mitochondrial toxicity; lipoatrophy See NRTI drug class effects, above. Malaise, headache, insomnia, seizures, myalgias. Anemia, granulocytopenia, thrombocytopenia; macrocytosis is an expected effect of zidovudine therapy and requires no intervention. Toxic myopathy with elevated creatine phosphokinase [CPK] ; with long-term use. Blue to black discoloration of nails and skin in pigmented races Drug interactions Careful monitoring required when used with other myelosuppressive drugs ie, trimethoprim-sulfamethoxazole, ganciclovir ; . Probenecid can increase levels of zidovudine. Acetaminophen Tylenol ; administration does not increase zidovudine toxicity. Avoid concomitant use with ribavirin Until efficacy wanes or toxicity occurs See NRTI drug class effects, above. Pancreatitis; painful peripheral neuropathy dosage related, reversible abdominal cramps, diarrhea related to antacid in formulation; rash; hyperglycemia; hyperuricemia; headache, insomnia, seizures; elevated triglyceride and amylase levels; thrombocytopenia; retinal atrophy Drug interactions Avoid alcohol and other pancreatic toxins eg, systemic pentamidine ; . Avoid concomitant neurotoxic drugs eg, zalcitabine, vinca alkaloids, oral ganciclovir ; . Decreases absorption of drugs whose absorption is impaired by buffered products eg, ketoconazole, itraconazole, indinavir, lopinavir, delavirdine, ritonavir, tetracyclines, quinolone antibiotics ; . Oral and intravenous ganciclovir might increase didanosine toxicity. Consider increasing didanosine dosage with methadone use Monitor for signs of zidovudine toxicity and reduce dosage if required. Transfusions or erythropoietin if endogenous erythropoietin level 500 IU L ; therapy can be used if anemia eg, hemoglobin 8.0 g dL ; occurs in patients who require zidovudine therapy. Decrease dosage or interrupt for absolute neutrophil count ANC ; 500 L; consider granulocyte colony-stimulating factor G-CSF ; . Transfusions and erythropoietin and G-CSF therapies are expensive; changing to alternate NRTI preferred High-dosage 1200 mg po qd ; zidovudine therapy can be considered for HIV dementia and thrombocytopenia. Toxicity of highdosage zidovudine can be substantial Monitor for signs of neuropathy. Two buffered tablets must be given per dose to provide adequate buffer for absorption. Can be difficult to chew; tablets do not dissolve readily in water, can be crushed manually or given with apple juice Administer didanosine on empty stomach 2 hours apart from antacids, H2 antagonists, and drugs eg, ketoconazole, itraconazole, indinavir, lopinavir, ritonavir, tetracyclines, delavirdine, quinolone antibiotics ; whose absorption is impaired by buffered products Enteric-coated capsules might cause less diarrhea and fewer drug interactions Didanosine plus stavudine combination should not be given to pregnant women because of increased risk of fatal lactic acidosis and indinavir.

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