No description available.

Objetivo:Existemevidências crescentes na literatura da participação do estresseoxidativonaprogressão e agressividade da endometriose. Nesse estudoprospectivo e controlado, foram medidos seis marcadores de estresse oxidativo com a finalidade de relacioná-los com a severidade e progressão da endometriose além debuscarum marcador diagnóstico para a doença. Pacientes e Métodos:Entre Julho de 2010 e Agosto de 2011, 62 pacientes consecutivas com diagnóstico histológico de endometriose foram identificadas como elegíveis para esse estudo. Após os critérios de exclusão, 44 pacientes foram alocadas em três grupos: Grupo A (estádios I/II da ASRM/1996), (n=14), grupo B (estádios III/IV da ASRM/1996),(n=16) e grupo controle (n=14). Os seguintes marcadores foram avaliados no fluido peritoneal e no tecido com endometriose: 8-hidroxi-2- deoxiguanosina (8-OHdG), 8-oxo-guaninaglicosilase (OGG1),proteínacarbonil (PC), oxidação lipídica (LPO), espécies reativas de oxigênio (ROS); capacidade totalantioxidante (TAC). Resultados: Observou-se elevação estatisticamente significante do 8 OhdG e da PC. Notou-se diminuição significativa na expressão do reparo de DNA (OGG1) em estádios avançados de endometriose. (p<0.001, p=0.001, p=0.033 respectivamente). Não notamos significância estatística entre os três grupos estudados nos marcadores ROS,CAT e LPO. Utilizando-se um modelo estatístico multivariável e as curvas ReceiverOperatingCharacteristics(ROC) construiu-se um modelo preditivo de severidade de doença. A habilidade do modelo de distinguir 16 entre os grupos A, B e o grupo controlefoi alta. O modelo foi capaz de diferenciar aproximadamente 9 em cada 10 pacientes incluídas (acerto/corrido foi de 87%). Conclusão:O aumento da lesão no DNA e a diminuição da atividade enzimática de reparo de DNA podem estar relacionados com a progressão da endometriose. Nossos resultados indicam que marcadores oxidativos de agressão celular podem se tornar testes valiosospara se verificar a severidade da endometriose / Objective: There is increasing evidence that oxidative stress is one of the key factors for endometriosis progression. In this prospective controlled trial, we measured six different biomarkers of oxidative stress targeting protein, lipid and DNA to quantify the severity and progression of endometriosis and establish a diagnostic marker for the disease. Methods: 62 consecutive patients were identified to be enrolled in this study. After exclusion criteria, 44 patients were allocated in three groups: Group A (Stage I/II - ASRM/1996), (n=14), Group B(Stage III/IV ASRM/1996), (n=16), and control group (n=14). Levels of 8 hydroxy- deoxyguanosine (8 OHdG), 8- oxoguanine DNA glycosylase (OGG1), protein carbonyl (PC), lipid peroxidation (LPO), reactive oxygen species (ROS); total antioxidant capacity (TAC) were accessed in peritoneal fluid and tissue. Results: 8-OhdG and PC levels were found to be significantly higher in patients with endometriosis, in addition OGG1 expression was found to be significantly lower in patients with endometriosis (p<0.001, p=0.001, p=0.033 respectively); however, stages I/II, stages III/IV, and control group showed comparable levels of ROS, TAC and LPO. A predictive model was built using multivariable analyses and receiver operating characteristics curves. The ability to predict and distinguish between groups A, B and control patients washigh. The model was corrected in proximally 9 out of 10 patients included (Model/Corrected ratio was 87%). Conclusion: Higher level of DNA damage and 19 lower expression of DNA repair activity may be related with endometriosis progression. Our results indicate that oxidative stress as a biomarker of cell injury might be a useful and reliable quantitative test of endometriosis severity

Objetivo:Existemevidências crescentes na literatura da participação do estresseoxidativonaprogressão e agressividade da endometriose. Nesse estudoprospectivo e controlado, foram medidos seis marcadores de estresse oxidativo com a finalidade de relacioná-los com a severidade e progressão da endometriose além debuscarum marcador diagnóstico para a doença. Pacientes e Métodos:Entre Julho de 2010 e Agosto de 2011, 62 pacientes consecutivas com diagnóstico histológico de endometriose foram identificadas como elegíveis para esse estudo. Após os critérios de exclusão, 44 pacientes foram alocadas em três grupos: Grupo A (estádios I/II da ASRM/1996), (n=14), grupo B (estádios III/IV da ASRM/1996),(n=16) e grupo controle (n=14). Os seguintes marcadores foram avaliados no fluido peritoneal e no tecido com endometriose: 8-hidroxi-2- deoxiguanosina (8-OHdG), 8-oxo-guaninaglicosilase (OGG1),proteínacarbonil (PC), oxidação lipídica (LPO), espécies reativas de oxigênio (ROS); capacidade totalantioxidante (TAC). Resultados: Observou-se elevação estatisticamente significante do 8 OhdG e da PC. Notou-se diminuição significativa na expressão do reparo de DNA (OGG1) em estádios avançados de endometriose. (p<0.001, p=0.001, p=0.033 respectivamente). Não notamos significância estatística entre os três grupos estudados nos marcadores ROS,CAT e LPO. Utilizando-se um modelo estatístico multivariável e as curvas ReceiverOperatingCharacteristics(ROC) construiu-se um modelo preditivo de severidade de doença. A habilidade do modelo de distinguir 16 entre os grupos A, B e o grupo controlefoi alta. O modelo foi capaz de diferenciar aproximadamente 9 em cada 10 pacientes incluídas (acerto/corrido foi de 87%). Conclusão:O aumento da lesão no DNA e a diminuição da atividade enzimática de reparo de DNA podem estar relacionados com a progressão da endometriose. Nossos resultados indicam que marcadores oxidativos de agressão celular podem se tornar testes valiosospara se verificar a severidade da endometriose / Objective: There is increasing evidence that oxidative stress is one of the key factors for endometriosis progression. In this prospective controlled trial, we measured six different biomarkers of oxidative stress targeting protein, lipid and DNA to quantify the severity and progression of endometriosis and establish a diagnostic marker for the disease. Methods: 62 consecutive patients were identified to be enrolled in this study. After exclusion criteria, 44 patients were allocated in three groups: Group A (Stage I/II - ASRM/1996), (n=14), Group B(Stage III/IV ASRM/1996), (n=16), and control group (n=14). Levels of 8 hydroxy- deoxyguanosine (8 OHdG), 8- oxoguanine DNA glycosylase (OGG1), protein carbonyl (PC), lipid peroxidation (LPO), reactive oxygen species (ROS); total antioxidant capacity (TAC) were accessed in peritoneal fluid and tissue. Results: 8-OhdG and PC levels were found to be significantly higher in patients with endometriosis, in addition OGG1 expression was found to be significantly lower in patients with endometriosis (p<0.001, p=0.001, p=0.033 respectively); however, stages I/II, stages III/IV, and control group showed comparable levels of ROS, TAC and LPO. A predictive model was built using multivariable analyses and receiver operating characteristics curves. The ability to predict and distinguish between groups A, B and control patients washigh. The model was corrected in proximally 9 out of 10 patients included (Model/Corrected ratio was 87%). Conclusion: Higher level of DNA damage and 19 lower expression of DNA repair activity may be related with endometriosis progression. Our results indicate that oxidative stress as a biomarker of cell injury might be a useful and reliable quantitative test of endometriosis severity

O câncer é a segunda maior causa de morte no mundo, sendo responsável por aproximadamente 7,6 milhões de óbitos. Entretanto, pesquisadores alertam para uma associação inversa entre o consumo de frutas e hortaliças e o desenvolvimento de neoplasias, desta forma a organização mundial da saúde sugere, dentre outras medidas para controle do câncer, o aumento do consumo de frutas e hortaliças. Nesse contexto o objetivo deste trabalho foi avaliar os eventuais efeitos quimiopreventivos das hortaliças Brassicas, couve (C) e repolho (R). Realizaram-se dois experimentos sendo o primeiro, o modelo de hepatocacinogênese de Ito, onde as hortaliças foram fornecidas durante 8 semanas na água de beber (10% p/v), animais que receberam apenas água foram utilizados como controle. Nesse experimento não houve inibição (P>0,05) de lesões pré-neoplásicas hepáticas positivas para glutationa S-transferase forma placental e não houve indução (P>0,05) da apoptose nos grupos tratados com C ou R. Contudo, observou-se redução (P<0,05) de danos em DNA hepático e aumento (P<0,05) da concentração hepática de luteína de ratos tratados com C e R, quando comparados a ratos controle. No segundo experimento as hortaliças foram fornecidas durante 8 semanas na água de beber (20% p/v), e os animais foram submetidos a aplicação do carcinogênico hepático 24h antes da eutanásia. Não houve redução (P>0,05) de danos em DNA, contudo a concentração do aduto de DNA 8-hidroxi-2-deoxiguanosina (8-OHdG) e foi elevada (P<0,05) em animais tratados com R quando comparados a tratados com C e controles. Com relação à expressão diferencial de genes, 29 genes foram diferencialmente expressos em fígado, dentre eles o gene da 8-oxoguanina-DNA-glicosilase (enzima de reparo do DNA), foi hipoexpressa no grupo tratado com R, o que pode explicar o aumentado valor de adutos no mesmo grupo. O cólon apresentou 31 genes com diferença de expressão, onde 5 genes estão relacionados ao metabolismo de xenobióticos. / Cancer is the major cause of death in the world, being responsible for approximately 7.6 million deaths. However, there is a hypothesis of an inverse association between fruit and vegetable consumption and the development of cancer. Therefore, the World Health Organization suggests, among other actions for controlling cancer, the increase in vegetable and fruit consumption. The aim of this work was to evaluate eventual chemopreventive effects of Brassicas vegetables, kale (K) and cabbage (C). Two experiments were done: the first one was Ito´s hepatocarcinogenesis model, where vegetables were provided during 8 weeks in the rats´ drinking water (10% w/v). Animals that received only water were considered control. In this experiment, there was no inhibition (P<0,05) of glutathione S-transferase placental form positive preneoplastic lesions and, also, there was no induction (P<0,05) of apoptosis in the groups treated with K or C However, it was observed a reduction (P<0,05) in hepatic DNA damages and an increase (P<0,05) in lutein hepatic concentration of rats treated with K or C, when compared to the control. In the second experiment, the vegetables were provided during 8 weeks in the rats´ drinking water (20% w/v), and animals were submitted to carcinogenic application 24h before euthanasia. There was no reduction (P<0,05) in DNA damages, however there was an increase (P<0,05) in the concentration of 8-hydroxy-2-deoxyguanosine (8-OHdG) DNA in animals treated with C when compared to the ones treated with K and control. In relation to the differential gene expression, 29 genes were differently expressed in the liver, such as the 8-oxoguanine-DNA-glycosylase gene, which was downregulated in the group treated with C. This might explain the increased value of adducts in the same group. Colon presented 31 genes with difference in expression, whereas 5 genes are related to xenobiotic metabolism.

The human body has evolved certain defence mechanisms to cope with the high occurrence of free radicals. These radicals are obtained endogenously from the mitochondria, peroxisomes, the cytochrome P450 (CYP 450) system and neutrophils, or exogenously from the environment. Lack of antioxidants and/or increased production of free radicals will result in oxidative stress, which has been implicated in certain human diseases such as hypertension, inflammation, ageing, autoimmunity, atherosclerosis, Parkinson?s disease, cancer and diabetes. Although the initial aim was to standardise a single assay to quantify both 8–OHdG and DHN–MA, this could not be achieved in this study due to the vast difference in the chemical properties of these two metabolites. Following the decision to use two separate assays for the quantification of the mentioned biomarkers, the 8–OHdG assay was standardised and validated. The intrabatch variation of the assay was 4.18% and the interbatch variation was 17.37%. Unfortunately, the DHN–MA assay could not be standardised within the time frame of this study due to experimental difficulties. Therefore, only urinary 8–OHdG and serum ROS levels were quantified. Urinary 8–OHdG levels were measured in 409 participants (209 Caucasians, 101 males and 108 females and 200 Africans, 100 males and 100 females) from the SABPA study. After removal of outliers from the data matrix, the effect of gender and ethnicity was investigated on the measured urinary 8–OHdG levels. No significant difference in the urinary 8–OHdG levels between Caucasian males (n=87) and females (n=96) were observed (p = 0.68). A similar observation was made for the African males (n=86) and females (n=84), where no significant difference in 8–OHdG levels was detected (p = 0.053). Thus, from the results obtained in this study, it seems that urinary 8–OHdG levels are not influenced by gender. However, 8–OHdG levels were dramatically influenced by ethnicity. Caucasian males (n=87) excreted 70% higher amounts of 8–OHdG compared to African males (n=86) (p < 0.001). Caucasian females (n=96) also excreted larger urinary 8–OHdG amounts (42%) compared to African females (n=84) (p < 0.001). Therefore, it seems that urinary 8–OHdG levels are dramatically influenced by ethnicity. Finally, urinary 8–OHdG levels were compared to serum ROS levels, but no significant correlation between the measured metabolites was observed (r = –0.045). Hence, urinary 8–OHdG and serum ROS levels are not related in these subjects. Even though the initial aim of this study was to standardise an analytical method to quantify both urinary 8–OHdG and DHN–MA, this could not be achieved due to time constraints. vi The human body has evolved certain defence mechanisms to cope with the high occurrence of free radicals. These radicals are obtained endogenously from the mitochondria, peroxisomes, the cytochrome P450 (CYP 450) system and neutrophils, or exogenously from the environment. Lack of antioxidants and/or increased production of free radicals will result in oxidative stress, which has been implicated in certain human diseases such as hypertension, inflammation, ageing, autoimmunity, atherosclerosis, Parkinson?s disease, cancer and diabetes. Although the initial aim was to standardise a single assay to quantify both 8–OHdG and DHN–MA, this could not be achieved in this study due to the vast difference in the chemical properties of these two metabolites. Following the decision to use two separate assays for the quantification of the mentioned biomarkers, the 8–OHdG assay was standardised and validated. The intrabatch variation of the assay was 4.18% and the interbatch variation was 17.37%. Unfortunately, the DHN–MA assay could not be standardised within the time frame of this study due to experimental difficulties. Therefore, only urinary 8–OHdG and serum ROS levels were quantified. Urinary 8–OHdG levels were measured in 409 participants (209 Caucasians, 101 males and 108 females and 200 Africans, 100 males and 100 females) from the SABPA study. After removal of outliers from the data matrix, the effect of gender and ethnicity was investigated on the measured urinary 8–OHdG levels. No significant difference in the urinary 8–OHdG levels between Caucasian males (n=87) and females (n=96) were observed (p = 0.68). A similar observation was made for the African males (n=86) and females (n=84), where no significant difference in 8–OHdG levels was detected (p = 0.053). Thus, from the results obtained in this study, it seems that urinary 8–OHdG levels are not influenced by gender. However, 8–OHdG levels were dramatically influenced by ethnicity. Caucasian males (n=87) excreted 70% higher amounts of 8–OHdG compared to African males (n=86) (p < 0.001). Caucasian females (n=96) also excreted larger urinary 8–OHdG amounts (42%) compared to African females (n=84) (p < 0.001). Therefore, it seems that urinary 8–OHdG levels are dramatically influenced by ethnicity. Finally, urinary 8–OHdG levels were compared to serum ROS levels, but no significant correlation between the measured metabolites was observed (r = –0.045). Hence, urinary 8–OHdG and serum ROS levels are not related in these subjects. Even though the initial aim of this study was to standardise an analytical method to quantify both urinary 8–OHdG and DHN–MA, this could not be achieved due to time constraints. However, an LC–MS/MS analytical assay was standardised and validated for the quantification of urinary 8–OHdG. The method proved reliable for the quantification of 8–OHdG from urine samples and can thus be used for further studies on oxidative DNA damage. / Thesis (M.Sc. (Biochemistry))--North-West University, Potchefstroom Campus, 2011.

The human body has evolved certain defence mechanisms to cope with the high occurrence of free radicals. These radicals are obtained endogenously from the mitochondria, peroxisomes, the cytochrome P450 (CYP 450) system and neutrophils, or exogenously from the environment. Lack of antioxidants and/or increased production of free radicals will result in oxidative stress, which has been implicated in certain human diseases such as hypertension, inflammation, ageing, autoimmunity, atherosclerosis, Parkinson?s disease, cancer and diabetes. Although the initial aim was to standardise a single assay to quantify both 8–OHdG and DHN–MA, this could not be achieved in this study due to the vast difference in the chemical properties of these two metabolites. Following the decision to use two separate assays for the quantification of the mentioned biomarkers, the 8–OHdG assay was standardised and validated. The intrabatch variation of the assay was 4.18% and the interbatch variation was 17.37%. Unfortunately, the DHN–MA assay could not be standardised within the time frame of this study due to experimental difficulties. Therefore, only urinary 8–OHdG and serum ROS levels were quantified. Urinary 8–OHdG levels were measured in 409 participants (209 Caucasians, 101 males and 108 females and 200 Africans, 100 males and 100 females) from the SABPA study. After removal of outliers from the data matrix, the effect of gender and ethnicity was investigated on the measured urinary 8–OHdG levels. No significant difference in the urinary 8–OHdG levels between Caucasian males (n=87) and females (n=96) were observed (p = 0.68). A similar observation was made for the African males (n=86) and females (n=84), where no significant difference in 8–OHdG levels was detected (p = 0.053). Thus, from the results obtained in this study, it seems that urinary 8–OHdG levels are not influenced by gender. However, 8–OHdG levels were dramatically influenced by ethnicity. Caucasian males (n=87) excreted 70% higher amounts of 8–OHdG compared to African males (n=86) (p < 0.001). Caucasian females (n=96) also excreted larger urinary 8–OHdG amounts (42%) compared to African females (n=84) (p < 0.001). Therefore, it seems that urinary 8–OHdG levels are dramatically influenced by ethnicity. Finally, urinary 8–OHdG levels were compared to serum ROS levels, but no significant correlation between the measured metabolites was observed (r = –0.045). Hence, urinary 8–OHdG and serum ROS levels are not related in these subjects. Even though the initial aim of this study was to standardise an analytical method to quantify both urinary 8–OHdG and DHN–MA, this could not be achieved due to time constraints. vi The human body has evolved certain defence mechanisms to cope with the high occurrence of free radicals. These radicals are obtained endogenously from the mitochondria, peroxisomes, the cytochrome P450 (CYP 450) system and neutrophils, or exogenously from the environment. Lack of antioxidants and/or increased production of free radicals will result in oxidative stress, which has been implicated in certain human diseases such as hypertension, inflammation, ageing, autoimmunity, atherosclerosis, Parkinson?s disease, cancer and diabetes. Although the initial aim was to standardise a single assay to quantify both 8–OHdG and DHN–MA, this could not be achieved in this study due to the vast difference in the chemical properties of these two metabolites. Following the decision to use two separate assays for the quantification of the mentioned biomarkers, the 8–OHdG assay was standardised and validated. The intrabatch variation of the assay was 4.18% and the interbatch variation was 17.37%. Unfortunately, the DHN–MA assay could not be standardised within the time frame of this study due to experimental difficulties. Therefore, only urinary 8–OHdG and serum ROS levels were quantified. Urinary 8–OHdG levels were measured in 409 participants (209 Caucasians, 101 males and 108 females and 200 Africans, 100 males and 100 females) from the SABPA study. After removal of outliers from the data matrix, the effect of gender and ethnicity was investigated on the measured urinary 8–OHdG levels. No significant difference in the urinary 8–OHdG levels between Caucasian males (n=87) and females (n=96) were observed (p = 0.68). A similar observation was made for the African males (n=86) and females (n=84), where no significant difference in 8–OHdG levels was detected (p = 0.053). Thus, from the results obtained in this study, it seems that urinary 8–OHdG levels are not influenced by gender. However, 8–OHdG levels were dramatically influenced by ethnicity. Caucasian males (n=87) excreted 70% higher amounts of 8–OHdG compared to African males (n=86) (p < 0.001). Caucasian females (n=96) also excreted larger urinary 8–OHdG amounts (42%) compared to African females (n=84) (p < 0.001). Therefore, it seems that urinary 8–OHdG levels are dramatically influenced by ethnicity. Finally, urinary 8–OHdG levels were compared to serum ROS levels, but no significant correlation between the measured metabolites was observed (r = –0.045). Hence, urinary 8–OHdG and serum ROS levels are not related in these subjects. Even though the initial aim of this study was to standardise an analytical method to quantify both urinary 8–OHdG and DHN–MA, this could not be achieved due to time constraints. However, an LC–MS/MS analytical assay was standardised and validated for the quantification of urinary 8–OHdG. The method proved reliable for the quantification of 8–OHdG from urine samples and can thus be used for further studies on oxidative DNA damage. / Thesis (M.Sc. (Biochemistry))--North-West University, Potchefstroom Campus, 2011.

O câncer é a segunda maior causa de morte no mundo, sendo responsável por aproximadamente 7,6 milhões de óbitos. Entretanto, pesquisadores alertam para uma associação inversa entre o consumo de frutas e hortaliças e o desenvolvimento de neoplasias, desta forma a organização mundial da saúde sugere, dentre outras medidas para controle do câncer, o aumento do consumo de frutas e hortaliças. Nesse contexto o objetivo deste trabalho foi avaliar os eventuais efeitos quimiopreventivos das hortaliças Brassicas, couve (C) e repolho (R). Realizaram-se dois experimentos sendo o primeiro, o modelo de hepatocacinogênese de Ito, onde as hortaliças foram fornecidas durante 8 semanas na água de beber (10% p/v), animais que receberam apenas água foram utilizados como controle. Nesse experimento não houve inibição (P>0,05) de lesões pré-neoplásicas hepáticas positivas para glutationa S-transferase forma placental e não houve indução (P>0,05) da apoptose nos grupos tratados com C ou R. Contudo, observou-se redução (P<0,05) de danos em DNA hepático e aumento (P<0,05) da concentração hepática de luteína de ratos tratados com C e R, quando comparados a ratos controle. No segundo experimento as hortaliças foram fornecidas durante 8 semanas na água de beber (20% p/v), e os animais foram submetidos a aplicação do carcinogênico hepático 24h antes da eutanásia. Não houve redução (P>0,05) de danos em DNA, contudo a concentração do aduto de DNA 8-hidroxi-2-deoxiguanosina (8-OHdG) e foi elevada (P<0,05) em animais tratados com R quando comparados a tratados com C e controles. Com relação à expressão diferencial de genes, 29 genes foram diferencialmente expressos em fígado, dentre eles o gene da 8-oxoguanina-DNA-glicosilase (enzima de reparo do DNA), foi hipoexpressa no grupo tratado com R, o que pode explicar o aumentado valor de adutos no mesmo grupo. O cólon apresentou 31 genes com diferença de expressão, onde 5 genes estão relacionados ao metabolismo de xenobióticos. / Cancer is the major cause of death in the world, being responsible for approximately 7.6 million deaths. However, there is a hypothesis of an inverse association between fruit and vegetable consumption and the development of cancer. Therefore, the World Health Organization suggests, among other actions for controlling cancer, the increase in vegetable and fruit consumption. The aim of this work was to evaluate eventual chemopreventive effects of Brassicas vegetables, kale (K) and cabbage (C). Two experiments were done: the first one was Ito´s hepatocarcinogenesis model, where vegetables were provided during 8 weeks in the rats´ drinking water (10% w/v). Animals that received only water were considered control. In this experiment, there was no inhibition (P<0,05) of glutathione S-transferase placental form positive preneoplastic lesions and, also, there was no induction (P<0,05) of apoptosis in the groups treated with K or C However, it was observed a reduction (P<0,05) in hepatic DNA damages and an increase (P<0,05) in lutein hepatic concentration of rats treated with K or C, when compared to the control. In the second experiment, the vegetables were provided during 8 weeks in the rats´ drinking water (20% w/v), and animals were submitted to carcinogenic application 24h before euthanasia. There was no reduction (P<0,05) in DNA damages, however there was an increase (P<0,05) in the concentration of 8-hydroxy-2-deoxyguanosine (8-OHdG) DNA in animals treated with C when compared to the ones treated with K and control. In relation to the differential gene expression, 29 genes were differently expressed in the liver, such as the 8-oxoguanine-DNA-glycosylase gene, which was downregulated in the group treated with C. This might explain the increased value of adducts in the same group. Colon presented 31 genes with difference in expression, whereas 5 genes are related to xenobiotic metabolism.

Point-of-care testing (POCT) is defined as medical testing at or near the site of patient care and has become a critical component of the diagnostic industry. POCT has many advantages over tests in centralized laboratories including small reagent volumes, small size, rapid turnaround time, cost-effectiveness, low power consumption and functional integration of multiple devices. Paper-based POCT sensors are a new alternative technology for fabricating simple, low-cost, portable and disposable analytical devices for clinical diagnosis. The focus of this dissertation was to develop simple, rapid and low cost paper-based POCT sensors with high sensitivity and portability for disease biomarker detection. Lateral flow strips (LFS) were used as the basic platform as it provides several key advantages such as simplicity, fast response time, on site and cost-effectiveness, and it can be used to detect specific substances including small molecules, large proteins and even whole pathogens, in a sample by immunological reactions. Earlier designs of paper strips lacked the quantitative information of the analyte concentration and could only provide single analyte detection at a time. In this study, a series of modifications were made to upgrade the platform to compensate for these limitations. First, we developed a gold nanoparticle based LFS for qualitative colorimetrical detection of bladder cancer related biomarkers in standard solutions and in urine samples. Second, by incorporating an image processing program “ImageJ”, a semi-quantitative LFS platform was established. The capability of the strip was evaluated by testing a small DNA oxidative damage biomarker in urine and cell culture models. Third, we combined the electrochemical method and colorimetrical method for quantitative biomarker detection. Finally, we integrated a commercialized blood glucose meter to quantitatively detection of two non-glucose biomarkers by converting their signals to that of glucose. The upgraded sensor could provide a noninvasive, rapid, visual, quantitative and convenient detection platform for various disease biomarkers. In addition, this platform does not require expensive equipments or trained personnel, deeming it suitable for use as a simple, economical and portable field kit for on-site biomarker monitoring in a variety of clinical settings.

No description available.