Asthma is a serious respiratory disease that is affected by environmental and psychological variables. Asthma education programs are used to reduce the morbidity associated with asthma and to teach people how to better manage their illness so that they might have a higher quality of life. Although much research has examined the effectiveness of asthma education programs within the Caucasian community, no research has been done to see if asthma education programs are effective in the Hispanic community. This study examined the effects of an asthma education program directed towards three Spanish-speaking parents of children, 7–17 years old, who were diagnosed with asthma. Participants were recruited from local health clinics with written advertisements and were given a monetary reward for their participation in the study. This study was a series of AB designs with staggered baselines, as well as pre and post testing. The pretests and posttests include translated checklists that measure knowledge, self-efficacy, symptoms, problem behaviors, and quality of life of caretakers of children with asthma. Data were also collected on the number of doctor visits and asthma attacks. Treatment consisted of a 2-hr asthma education intervention in Spanish for the parents and caretakers of asthmatic children. It was expected that symptoms, number of doctor visits, number of asthma attacks, and problem behaviors would decline and that knowledge, self-efficacy and quality of life would increase for each of the participants. Only parent knowledge of asthma management techniques increased significantly after the implementation of the treatment. Implications of the study are discussed.

Several studies suggest that women are less likely to buy, carry, or keep condoms at home than men. This study assesses if women exposed to interventions supportive of buying and carrying condoms would have more favorable attitudes towards condoms and higher actual condom use than women exposed to general information regarding condom use. It also compared the effectiveness of modeling with modeling + role-play as condom buying/carrying interventions. Results were analyzed using a 3 (information, information + modeling, information + modeling + role play) x 2 (posttest/follow-up) split-plot ANOVA. There was no significant difference between groups, no significant differences between posttest and follow-up, and no significant interaction for any measure. The differences between groups approached significance for the CUSES. The Sexual History Questionnaire revealed significant changes on four of the behavioral items. Implications of the study are discussed.

This investigation focused on four aspects of hexamethylene bisacetamide's ( HMBA ) involvement in induction of differentiation in murine erythroleukemia (MEL) cells: (a) Effects of APAH , a N 8 -acetylspermidine deacetylase inhibitor, on differentiation induced by HMBA and its two deacetylated metabolites, NADAH and DAH , (b) influence of APAH on intracellular levels of HMBA and its deacetylated metabolites in HMBA treated MEL cells, (c) Ca 2+ mobilizing effects of HMBA, NADAH and DAH and (d) effect of APAH on HMBA induced changes in c- myc gene expression during differentiation. HMBA (5 mM) and DAH (2 mM) were equally effective in inducing MEL cell differentiation as measured by the amount of hemoglobin (Hb) produced, while NADAH (5 mM) was least effective. APAH (10–500 0μM) inhibited HMBA and NADAH induced differentiation without affecting DAH induced differentiation. APAH (500 μM) was shown to affect the deacetylation pathway for HMBA. There was a significant increase in intracellular NADAH levels and a decrease in DAH levels in MEL cells treated with both HMBA and APAH compared to HMBA alone (measured by LC/MS). This indicated that APAH inhibited the second deacetylation step, the conversion of NADAH to DAH but not the first, the conversion of HMBA to NADAH. Ca 2+ influx is necessary for HMBA induced MEL cell differentiation. BAPTA-AM (10 μM), a calcium chelator, inhibited HMBA induced Hb production while Tg (0.5 nM), the SERCA pump blocker, potentiated Hb production. 2-APB, a store operated channel (SOC) regulator, at higher concentrations (50,75 μM) prevented HMBA induced differentiation while at lower concentrations (5,10 μM) potentiated induced differentiation. DAH (0.5 mM), caused an immediate increase in [Ca 2+ ] i in MEL cells, while a slower response was seen with NADAH (3 mM). HMBA (5 mM) had the longest lag period (∼6 min) before it elevated [Ca 2+ ] i . APAH effectively prevented [Ca 2+ ] i increase caused by HMBA and NADAH but failed to alter DAH induced increase suggesting that DAH was the metabolite that raised [Ca 2+ ] i levels. Permeabilized cell assays demonstrated that DAH mobilized Ca 2+ from intracellular IP 3 sensitive stores in the ER. The identity of SOC for DAH induced Ca 2+ influx was inconclusive since 2-APB was not able to alter DAH induced Ca 2+ mobilizing responses. In addition to preventing HMBA induced MEL cell differentiation, APAH also inhibited the second phase of repression of c- myc gene expression, a hallmark of induced differentiation. In summary, the present study suggests the mechanism of action of HMBA requires the active involvement of a metabolite, DAH, in differentiation of hematopoietic cells.

Phenytoin is a relatively old anticonvulsant, but it has been commonly prescribed for more than half a century. The variability of phenytoin pharmacokinetic characteristics presents a challenge in therapeutic drug monitoring; hence, in the past twenty years its pharmacokinetic characteristics have been studied extensively. Up to now the studies were done with either healthy individuals or patients with normal liver functions. In this study a multifactorial scale of liver function, Pugh-Modified CTC (Child-Turcotte Criteria), has been incorporated to develop and evaluate a population pharmacokinetic model for phenytoin to be used in patients with liver dysfunction. Nonlinear Mixed Effects Model (NONMEM), a regression computer program, was utilized to develop the population pharmacokinetic model on the data of this study. The predictive performance of this model was evaluated by means of bootstrapping of the prediction error (PE) with the improved prediction-error (PE imp ) serving as an estimate of internal validity. The developed and validated final population pharmacokinetic model for phenytoin in patients with liver dysfunction is presented as follows: [special characters omitted] where Vmax is the maximum metabolic rate (mg/h); &thetas; 1 , the intercept for Vmax, is 7.41 mg/h; WT is the body weight (Kg); LS indicates one of three liver statuses: normal (CTC ≤ 6), mild dysfunction (CTC scores of 7–9), and moderate dysfunction (CTC scores of 10–12); Vd, the apparent volume of distribution (L), is 184 L; &thetas; WT is 0.126 and &thetas; LS is 2.14 for moderate liver-dysfunction. The maximum metabolic rate increased in patients with liver dysfunction, and there was weak statistical evidence that Vmax might increase in patients with chronic alcohol abuse. Based on the aforementioned longitudinal (population) pharmacokinetic model, a dosing method was also developed. By utilizing the dosing method, it may be possible to improve phenytoin dosage regimens, initial doses, and Bayesian estimates of pharmacokinetic parameters. Improved initial doses and more accurate estimates of pharmacokinetic parameters may lead to fewer required measured phenytoin concentrations and fewer dose changes. A decrease in the number of dose changes should result in less time expended in the writing and processing prescriptions and orders, and there may also be fewer wasted doses. Additionally, the improved initial doses should result in concentrations more frequently in the therapeutic window; thereby, resulting in less toxicity, greater efficacy, and improved patient compliance. All of these effects should decrease the cost of therapy in patients receiving phenytoin, a factor which is an important consideration in this age of cost containment and managed care.

The objective of this research was to investigate two important aspects of buccal drug delivery, transport and mucoadhesion. Buspirone was chosen as a model drug for the in vitro buccal transport studies, polyvinyl alcohol and sodium alginate polymer blends were prepared to investigate the mucoadhesive properties through a Lewis acid-base approach and finally, the effect of formulation factors on the force of mucoadhesion, surface energy parameters, release rate and flux was studied. In vitro permeation studies were conducted to investigate the buccal transport pathway of buspirone. Mathematical models were developed to quantify the process of permeation. Permeation enhancement of buspirone across the buccal mucosa was investigated using bile salts (sodium glycocholate and taurodeoxycholate), propylene glycol, propylene. Effect of formulation factors like drug, enhancer, and plasticizer was studied through statistically designed experiments. These experiments aided in characterizing the buccal delivery system. Mathematical models were developed for surface energy parameters, force of mucoadhesion, release rate, and flux. Research conducted in this dissertation focused on two important aspects of transbuccal delivery, drug transport and mucoadhesion by studying a model drug and polymer blends. The results obtained in these investigations can be utilized in the development of other bioadhesive delivery systems with respect to drug transport and mucoadhesion. Polymer blends of polyvinyl alcohol (PVA) and sodium alginate (Alg) were prepared to evaluate their mucoadhesive properties and investigate mucoadhesive mechanism by a Lewis acid-base approach. (Abstract shortened by UMI.)

Trichomonas vaginalis carries out unique mode of carbohydrate decarboxylation by an intracellular compartment, hydrogenosome. It was suggested that enzymes exclusively associated with hydrogenosome were responsible for activating metronidazole. This provoked researchers to target hydrogensosomal enzymes such as pyruvate: ferredoxin oxioreductase and ferredoxin, to treat trichomoniasis caused by T. vaginalis. Recent studies have shown alternative pathways responsible for activating metronidazole without the involvement of hydrogenosomal enzymes. This pathway requires the participation of thioredoxin and thioredoxin reductase. These enzymes are essential for T.vaginalis' survival as it is responsible for maintaining cell's redox system, as well as many other cellular processes. Targeting thioredoxin and thioredoxin reductase could be a novel drug target to treat metronidazole-resistant T. vaginalis. In this study, recombinant T. vaginalis TrxR and T. vaginalis Trx were produced to test its activity against known TrxR inhibitor, auranofin, using DTNB assay. Cell lysates of metronidazole susceptible and metronidazole resistant lines were also tested to see its activity against auranofin. Auranofin derivatives that were effective on E. histolytica recombinant TrxR were also tested to compare their effects on T. vaginalis recombinant TrxR. The results showed that auranofin effectively inhibits recombinant TvTrxR. Aurnofin derivatives were also shown to have different effects on inhibiting the activity of recombinant TvTrxR. It is known that auranofin also targets mammalian TrxR. With the degree of different inhibitions observed between auranofin derivatives, it opened the possibility of developing an auranofin derivative that can specifically targets thioredoxin reductase of parasitic protozoan, T. vaginalis.

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