Relevant bibliographies by topics / PBDs

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'PBDs'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "PBDs"

1

Dechent, Sarah-Elisabeth, Arjan W. Kleij, and Gerrit A. Luinstra. "Fully bio-derived CO2 polymers for non-isocyanate based polyurethane synthesis." Green Chemistry 22, no. 3 (2020): 969–78. http://dx.doi.org/10.1039/c9gc03488a.

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Jakše, Jakše, Pajek, and Pajek. "Uric Acid and Plant-Based Nutrition." Nutrients 11, no. 8 (July 26, 2019): 1736. http://dx.doi.org/10.3390/nu11081736.

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Plant-based diets (PBDs) are associated with decreased risk of morbidity and mortality associated with important noncommunicable chronic diseases. Similar to animal-based food sources (e.g., meat, fish, and animal visceral organs), some plant-based food sources (e.g., certain soy legume products, sea vegetables, and brassica vegetables) also contain a high purine load. Suboptimally designed PBDs might consequently be associated with increased uric acid levels and gout development. Here, we review the available data on this topic, with a great majority of studies showing reduced risk of hyperuricemia and gout with vegetarian (especially lacto-vegetarian) PBDs. Additionally, type of ingested purines, fiber, vitamin C, and certain lifestyle factors work in concordance to reduce uric acid generation in PBDs. Recent limited data show that even with an exclusive PBD, uric acid concentrations remain in the normal range in short- and long-term dieters. The reasonable consumption of plant foods with a higher purine content as a part of PBDs may therefore be safely tolerated in normouricemic individuals, but additional data is needed in hyperuricemic individuals, especially those with chronic kidney disease.
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Abel, R. J. R., and F. E. Bennett. "Quintessential PBDs and PBDs with prime power block sizes ≥ 8." Journal of Combinatorial Designs 13, no. 4 (2005): 239–67. http://dx.doi.org/10.1002/jcd.20036.

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Al-Bahlani, Shadia, Buthaina Al-Dhahli, Kawther Al-Adawi, Abdurahman Al-Nabhani, and Mohamed Al-Kindi. "Platinum-Based Drugs Differentially Affect the Ultrastructure of Breast Cancer Cell Types." BioMed Research International 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/3178794.

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Breast cancer (BC) is the most common cause of cancer-related death worldwide. Although platinum-based drugs (PBDs) are effective anticancer agents, responsive patients eventually become resistant. While resistance of some cancers to PBDs has been explored, the cellular responses of BC cells are not studied yet. Therefore, we aim to assess the differential effects of PBDs on BC ultrastructure. Three representative cells were treated with different concentrations and timing of Cisplatin, Carboplatin, and Oxaliplatin. Changes on cell surface and ultrastructure were detected by scanning (SEM) and transmission electron microscope (TEM). In SEM, control cells were semiflattened containing microvilli with extending lamellipodia while treated ones were round with irregular surface and several pores, indicating drug entry. Prolonged treatment resembled distinct apoptotic features such as shrinkage, membrane blebs, and narrowing of lamellipodia with blunt microvilli. TEM detected PBDs’ deposits that scattered among cellular organelles inducing structural distortion, lumen swelling, chromatin condensation, and nuclear fragmentation. Deposits were attracted to fat droplets, explained by drug hydrophobic properties, while later they were located close to cell membrane, suggesting drug efflux. Phagosomes with destructed organelles and deposits were detected as defending mechanism. Understanding BC cells response to PBDs might provide new insight for an effective treatment.
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Elliott, Patrick S., Soraeya S. Kharaty, and Catherine M. Phillips. "Plant-Based Diets and Lipid, Lipoprotein, and Inflammatory Biomarkers of Cardiovascular Disease: A Review of Observational and Interventional Studies." Nutrients 14, no. 24 (December 17, 2022): 5371. http://dx.doi.org/10.3390/nu14245371.

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Plant-based diets (PBDs) are becoming increasingly popular. Thus far, the literature has focused on their association with lipid profiles, with less investigation of lipoprotein and inflammatory profiles. Because pro-atherogenic lipid, lipoprotein, and inflammatory processes may facilitate the development of atherosclerosis, understanding the relation between PBDs and these processes is important to inform risk mitigation strategies. Therefore, the objective of this paper was to review the literature on PBDs and lipid, lipoprotein, and inflammatory biomarkers of cardiovascular disease (CVD). A structured literature search was performed, retrieving 752 records, of which 43 articles were included. Plant-based diets generally associated with favourable lipid and lipoprotein profiles, characterised by decreased total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B concentrations, and less low-grade inflammation, characterised by decreased C-reactive protein concentrations. Effect sizes from PBD interventions were greatest compared to habitual dietary patterns, and for non-low-fat vegan and tightly controlled dietary interventions. Associations between PBD indices and the reviewed biomarkers were less consistent. Findings are discussed with reference to the literature on PBDs and PBD indices and CVD risk, the associations between specific plant food groups and CVD outcomes and the reviewed biomarker outcomes, and the potential mechanisms underpinning associations between PBDs and reduced CVD risk.
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Low, M. J. D., and C. Morterra. "Infrared Surface Studies of Opaque or Scattering Materials Using Photothermal Beam Deflection Spectroscopy." Adsorption Science & Technology 2, no. 2 (June 1985): 131–50. http://dx.doi.org/10.1177/026361748500200206.

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Infrared (IR) photothermal beam deflection spectroscopy (PBDS) is briefly described and some of its applications to studies of carbons and highly scattering materials are reviewed. PBDS is especially useful for the study of materials which absorb IR radiation very strongly or act as strong IR scatterers, so that conventional IR techniques fail. Application of PBDS to study the thermal degradation of a phenol-formaldehyde resin, the reaction of NH3 and H2O with the surfaces of intermediate-temperature chars, the effect of Fe3+ on the charring of cellulose, the dehydration of titanyl sulphate, and TiO2 pigments, are described.
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Austin, Grace, Jessica J. A. Ferguson, and Manohar L. Garg. "Effects of Plant-Based Diets on Weight Status in Type 2 Diabetes: A Systematic Review and Meta-Analysis of Randomised Controlled Trials." Nutrients 13, no. 11 (November 16, 2021): 4099. http://dx.doi.org/10.3390/nu13114099.

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Excessive adiposity is a major risk factor for type 2 diabetes (T2D), and dietary patterns are important determinants of weight status. Plant-based dietary patterns (PBDs) are known for their therapeutic effects on T2D. The aim is to systematically review RCTs to investigate the effects of various PBDs compared to regular meat-eating diets (RMDs), in individuals who normally consume a RMD on body weight, BMI, and waist circumference in T2D. RCTs investigating PBDs and body weight, BMI, WC for ≥6 weeks in adults with T2D since 1980 were eligible for inclusion. Seven trials (n = 269) were included in the meta-analysis using random-effects models and expressed as MD (95%Cls). Compared to RMDs, PBDs significantly lowered body weight (−2.35 kg, 95% CI: −3.51, −1.19, p < 0.001), BMI (−0.90 kg/m2, 95% CI: −1.42, −0.38, p = 0.001) and WC (−2.41 cm, 95% CI: −3.72, −1.09, p < 0.001). PBDs alone significantly reduced body weight by 5.1% (−4.95 kg, 95% CI: −7.34, −2.55, p < 0.001), BMI by 5.4% (−1.87 kg/m2, 95% CI: −2.78, −0.95, p < 0.001) and WC by 4.3%(−4.23, 95% CI: −6.38, −2.07, p < 0.001). Interventions not limiting energy intake led to a significant reduction in body weight (−2.54 kg, 95% CI: −4.16, −0.92, p < 0.005) and BMI (−0.91 kg/m2, 95% CI: −1.56, −0.25, p < 0.005). Trials ≥16 weeks had a pronounced reduction in body weight (−2.93 kg, 95% CI: −5.00, −0.87, p = 0.005) and BMI (−1.13 kg/m2, 95% CI: −1.89, −0.38, p < 0.005). These findings provide evidence for the implementation of PBDs for better management of central adiposity in individuals with T2D.
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Gibbs, Joshua, and Francesco P. Cappuccio. "Plant-Based Dietary Patterns for Human and Planetary Health." Nutrients 14, no. 8 (April 13, 2022): 1614. http://dx.doi.org/10.3390/nu14081614.

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The coronavirus pandemic has acted as a reset on global economies, providing us with the opportunity to build back greener and ensure global warming does not surpass 1.5 °C. It is time for developed nations to commit to red meat reduction targets and shift to plant-based dietary patterns. Transitioning to plant-based diets (PBDs) has the potential to reduce diet-related land use by 76%, diet-related greenhouse gas emissions by 49%, eutrophication by 49%, and green and blue water use by 21% and 14%, respectively, whilst garnering substantial health co-benefits. An extensive body of data from prospective cohort studies and controlled trials supports the implementation of PBDs for obesity and chronic disease prevention. The consumption of diets high in fruits, vegetables, legumes, whole grains, nuts, fish, and unsaturated vegetable oils, and low in animal products, refined grains, and added sugars are associated with a lower risk of all-cause mortality. Meat appreciation, health concerns, convenience, and expense are prominent barriers to PBDs. Strategic policy action is required to overcome these barriers and promote the implementation of healthy and sustainable PBDs.
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Vitetta, Luis, and Avni Sali. "Primary Bile Duct Stones and Bacterial Activity." HPB Surgery 6, no. 1 (January 1, 1992): 23–33. http://dx.doi.org/10.1155/1992/81017.

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The results of this study suggest that infection with beta-glucuronidase active bacteria is the initial event in the nucleation of primary bile duct stones (PBDS).PBDS from five patients were morphologically fragile and “earthy” with alternating light and dark brown pigment layers with no evidence of a distinct central nucleus that may have been reminiscent of a different structure. Chemically, calcium bilirubinate and calcium palmitate were prominent throughout their structure. All bile duct biles had a positive culture and were always associated with at least one bacterial species which was beta-glucuronidase active. Moreover, fragments of PBDS nuclear areas had positive cultures that were comparable with those present in their individual bile duct bile. Microscopic examination of bile showed abundant precipitation of calcium bilirubinate granules in all samples.Thus, bile duct bile infection with beta-glucuronidase active bacteria (e.g. E. coli, C. perfringens) appears to be a key factor in PBDS pathogenesis, having a precursor role, rather than being a consequence. Bile stasis is likely to be a co-factor which must have a supportive role in subsequent stone growth.
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Abe, Yuichi, Masanori Honsho, Ryota Itoh, Ryoko Kawaguchi, Masashi Fujitani, Kazushirou Fujiwara, Masaaki Hirokane, et al. "Peroxisome biogenesis deficiency attenuates the BDNF-TrkB pathway-mediated development of the cerebellum." Life Science Alliance 1, no. 6 (December 2018): e201800062. http://dx.doi.org/10.26508/lsa.201800062.

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Peroxisome biogenesis disorders (PBDs) manifest as neurological deficits in the central nervous system, including neuronal migration defects and abnormal cerebellum development. However, the mechanisms underlying pathogenesis remain enigmatic. Here, to investigate how peroxisome deficiency causes neurological defects of PBDs, we established a new PBD model mouse defective in peroxisome assembly factor Pex14p, termed Pex14ΔC/ΔC mouse. Pex14ΔC/ΔC mouse manifests a severe symptom such as disorganization of cortical laminar structure and dies shortly after birth, although peroxisomal biogenesis and metabolism are partially defective. The Pex14ΔC/ΔC mouse also shows malformation of the cerebellum including the impaired dendritic development of Purkinje cells. Moreover, extracellular signal-regulated kinase and AKT signaling are attenuated in this mutant mouse by an elevated level of brain-derived neurotrophic factor (BDNF) together with the enhanced expression of TrkB-T1, a dominant-negative isoform of the BDNF receptor. Our results suggest that dysregulation of the BDNF-TrkB pathway, an essential signaling for cerebellar morphogenesis, gives rise to the pathogenesis of the cerebellum in PBDs.
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Dissertations / Theses on the topic "PBDs"

1

Zioga, Georgia. "Studies on the reaction of pyrrolobenzodiazepines with nucleophiles." Thesis, University of Portsmouth, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298374.

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Narayanaswamy, Mathangi. "An Assay combining HPLC and MS to Evaluate the DNA-Interaction of Pyrrolobenzodiazepines (PBDs) with Oligonucleotides." Thesis, University College London (University of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509315.

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Nandigam, Harika. "Capability of the Tumor Microenvironment to Attract a Precursor of B-cells and Dendritic Cells from Bone Marrow." Ohio University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1307108043.

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Söderström, Gunilla. "On the combustion and photolytic degradation products of some brominated flame retardants." Doctoral thesis, Umeå University, Chemistry, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-107.

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Many modern products, especially electronic goods, are protected by brominated flame retardants (BFR). Some of the most common flame retardants are polybrominated diphenylethers (PBDE), tetrabromobisphenol-A (TBBP-A) and hexabromocyclododecane (HBCD). These compounds have been found in environmental samples and shown to have physiological effects on experimental animals. This thesis considers end-of-life aspects of brominated flame retardants. When spread in the environment, these compounds may be degraded into other forms. For example, if sludge contaminated with PBDE is used as an agricultural fertilizer, the PBDE could be degraded by sunlight to species of PBDE with lower degree of bromination and, to some extent, also form polybrominated dibenzofurans (PBDF). In addition, PBDF and polybrominated dibenzo-p-dioxins (PBDD) are formed during combustion of brominated flame retardants. When waste products with brominated flame retardants are co-combusted with household waste or other chlorinated fuel, polybrominated- chlorinated dibenzo-p-dioxins (PBCDD) and polybrominated- chlorinated dibenzofurans (PBCDF)will be formed. The bromin/chlorine composition of dioxins and furans is dependent on the bromine/chlorine ratio in the fuel, but the types of brominated flame retardants that are being combusted is less important. In the studies reported here, bromine levels higher than "normal" for household waste has been used. The results show that there is a pronounced increase in total dioxin levels in fluegas when when bromine is present, implying that waste containing brominated flame retardants should only be incinerated at combustion plants with effecient air pollution control devices.

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Maxwell, Megan Amanda, and n/a. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis." Griffith University. School of Biomolecular and Biomedical Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040219.100649.

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The peroxisome is a subcellular organelle that carries out a diverse range of metabolic functions, including the b-oxidation of very long chain fatty acids, the breakdown of peroxide and the a-oxidation of fatty acids. Disruption of peroxisome metabolic functions leads to severe disease in humans. These diseases can be broadly grouped into two categories: those in which a single enzyme is defective, and those known as the peroxisome biogenesis disorders (PBDs), which result from a generalised failure to import peroxisomal matrix proteins (and consequently result in disruption of multiple metabolic pathways). The PBDs result from mutations in PEX genes, which encode protein products called peroxins, required for the normal biogenesis of the peroxisome. PEX1 encodes an AAA ATPase that is essential for peroxisome biogenesis, and mutations in PEX1 are the most common cause of PBDs worldwide. This study focused on the identification of mutations in PEX1 in an Australasian cohort of PBD patients, and the impact of these mutations on PEX1 function. As a result of the studies presented in this thesis, twelve mutations in PEX1 were identified in the Australasian cohort of patients. The identified mutations can be broadly grouped into three categories: missense mutations, mutations directly introducing a premature termination codon (PTC) and mutations that interrupt the reading frame of PEX1. The missense mutations that were identified were R798G, G843D, I989T and R998Q; all of these mutations affect amino acid residues located in the AAA domains of the PEX1 protein. Two mutations that directly introduce PTCs into the PEX1 transcript (R790X and R998X), and four frameshift mutations (A302fs, I370fs, I700fs and S797fs) were identified. There was also one mutation found in an intronic region (IVS22-19A>G) that is presumed to affect splicing of the PEX1 mRNA. Three of these mutations, G843D, I700fs and G973fs, were found at high frequency in this patient cohort. At the commencement of these studies, it was hypothesised that missense mutations would result in attenuation of PEX1 function, but mutations that introduced PTCs, either directly or indirectly, would have a deleterious effect on PEX1 function. Mutations introducing PTCs are thought to cause mRNA to be degraded by the nonsense-mediated decay of mRNA (NMD) pathway, and thus result in a decrease in PEX1 protein levels. The studies on the cellular impact of the identified PEX1 mutations were consistent with these hypotheses. Missense mutations were found to reduce peroxisomal protein import and PEX1 protein levels, but a residual level of function remained. PTC-generating mutations were found to have a major impact on PEX1 function, with PEX1 mRNA and protein levels being drastically reduced, and peroxisomal protein import capability abolished. Patients with two missense mutations showed the least impact on PEX1 function, patients with two PTC-generating mutations had a severe defect in PEX1 function, and patients carrying a combination of a missense mutation and a PTC-generating mutation showed levels of PEX1 function that were intermediate between these extremes. Thus, a correlation between PEX1 genotype and phenotype was defined for the Australasian cohort of patients investigated in these studies. For a number of patients, mutations in the coding sequence of one PEX1 allele could not be identified. Analysis of the 5' UTR of this gene was therefore pursued for potential novel mutations. The initial analyses demonstrated that the 5' end of PEX1 extended further than previously reported. Two co-segregating polymorphisms were also identified, termed –137 T>C and –53C>G. The -137T>C polymorphism resided in an upstream, in-frame ATG (termed ATG1), and the possibility that the additional sequence represented PEX1 coding sequence was examined. While both ATGs were found to be functional by virtue of in vitro and in vivo expression investigations, Western blot analysis of the PEX1 protein in patient and control cell extracts indicated that physiological translation of PEX1 was from the second ATG only. Using a luciferase reporter approach, the additional sequence was found to exhibit promoter activity. When examined alone the -137T>C polymorphism exerted a detrimental effect on PEX1 promoter activity, reducing activity to half that of wild-type levels, and the -53C>G polymorphism increased PEX1 promoter activity by 25%. When co-expressed (mimicking the physiological condition) these polymorphisms compensated for each other to bring PEX1 promoter activity to near wild-type levels. The PEX1 mutations identified in this study have been utilised by collaborators at the National Referral Laboratory for Lysosomal, Peroxisomal and Related Genetic Disorders (based at the Women's and Children's Hospital, Adelaide), in prenatal diagnosis of the PBDs. In addition, the identification of three common mutations in Australasian PBD patients has led to the implementation of screening for these mutations in newly referred patients, often enabling a precise diagnosis of a PBD to be made. Finally, the strong correlation between genotype and phenotype for the patient cohort investigated as part of these studies has generated a basis for the assessment of newly identified mutations in PEX1.
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Maxwell, Megan Amanda. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis." Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366184.

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The peroxisome is a subcellular organelle that carries out a diverse range of metabolic functions, including the b-oxidation of very long chain fatty acids, the breakdown of peroxide and the a-oxidation of fatty acids. Disruption of peroxisome metabolic functions leads to severe disease in humans. These diseases can be broadly grouped into two categories: those in which a single enzyme is defective, and those known as the peroxisome biogenesis disorders (PBDs), which result from a generalised failure to import peroxisomal matrix proteins (and consequently result in disruption of multiple metabolic pathways). The PBDs result from mutations in PEX genes, which encode protein products called peroxins, required for the normal biogenesis of the peroxisome. PEX1 encodes an AAA ATPase that is essential for peroxisome biogenesis, and mutations in PEX1 are the most common cause of PBDs worldwide. This study focused on the identification of mutations in PEX1 in an Australasian cohort of PBD patients, and the impact of these mutations on PEX1 function. As a result of the studies presented in this thesis, twelve mutations in PEX1 were identified in the Australasian cohort of patients. The identified mutations can be broadly grouped into three categories: missense mutations, mutations directly introducing a premature termination codon (PTC) and mutations that interrupt the reading frame of PEX1. The missense mutations that were identified were R798G, G843D, I989T and R998Q; all of these mutations affect amino acid residues located in the AAA domains of the PEX1 protein. Two mutations that directly introduce PTCs into the PEX1 transcript (R790X and R998X), and four frameshift mutations (A302fs, I370fs, I700fs and S797fs) were identified. There was also one mutation found in an intronic region (IVS22-19A>G) that is presumed to affect splicing of the PEX1 mRNA. Three of these mutations, G843D, I700fs and G973fs, were found at high frequency in this patient cohort. At the commencement of these studies, it was hypothesised that missense mutations would result in attenuation of PEX1 function, but mutations that introduced PTCs, either directly or indirectly, would have a deleterious effect on PEX1 function. Mutations introducing PTCs are thought to cause mRNA to be degraded by the nonsense-mediated decay of mRNA (NMD) pathway, and thus result in a decrease in PEX1 protein levels. The studies on the cellular impact of the identified PEX1 mutations were consistent with these hypotheses. Missense mutations were found to reduce peroxisomal protein import and PEX1 protein levels, but a residual level of function remained. PTC-generating mutations were found to have a major impact on PEX1 function, with PEX1 mRNA and protein levels being drastically reduced, and peroxisomal protein import capability abolished. Patients with two missense mutations showed the least impact on PEX1 function, patients with two PTC-generating mutations had a severe defect in PEX1 function, and patients carrying a combination of a missense mutation and a PTC-generating mutation showed levels of PEX1 function that were intermediate between these extremes. Thus, a correlation between PEX1 genotype and phenotype was defined for the Australasian cohort of patients investigated in these studies. For a number of patients, mutations in the coding sequence of one PEX1 allele could not be identified. Analysis of the 5' UTR of this gene was therefore pursued for potential novel mutations. The initial analyses demonstrated that the 5' end of PEX1 extended further than previously reported. Two co-segregating polymorphisms were also identified, termed –137 T>C and –53C>G. The -137T>C polymorphism resided in an upstream, in-frame ATG (termed ATG1), and the possibility that the additional sequence represented PEX1 coding sequence was examined. While both ATGs were found to be functional by virtue of in vitro and in vivo expression investigations, Western blot analysis of the PEX1 protein in patient and control cell extracts indicated that physiological translation of PEX1 was from the second ATG only. Using a luciferase reporter approach, the additional sequence was found to exhibit promoter activity. When examined alone the -137T>C polymorphism exerted a detrimental effect on PEX1 promoter activity, reducing activity to half that of wild-type levels, and the -53C>G polymorphism increased PEX1 promoter activity by 25%. When co-expressed (mimicking the physiological condition) these polymorphisms compensated for each other to bring PEX1 promoter activity to near wild-type levels. The PEX1 mutations identified in this study have been utilised by collaborators at the National Referral Laboratory for Lysosomal, Peroxisomal and Related Genetic Disorders (based at the Women's and Children's Hospital, Adelaide), in prenatal diagnosis of the PBDs. In addition, the identification of three common mutations in Australasian PBD patients has led to the implementation of screening for these mutations in newly referred patients, often enabling a precise diagnosis of a PBD to be made. Finally, the strong correlation between genotype and phenotype for the patient cohort investigated as part of these studies has generated a basis for the assessment of newly identified mutations in PEX1.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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7

Löfstrand, Karin. "Trends and exposure of naturally produced brominated substances in Baltic biota - with focus on OH-PBDEs, MeO-PBDEs and PBDDs." Doctoral thesis, Stockholms universitet, Institutionen för material- och miljökemi (MMK), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-54421.

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The semi-enclosed and brackish Baltic Sea has become heavily polluted by nutrients, anthropogenic organic and inorganic chemicals via human activities. Persistent organic pollutants (POPs) have been thoroughly investigated due to their linkage to toxic effects observed in Baltic biota. There has been far less focus on semi-persistent pollutants e.g. naturally produced oraganohalogen compounds (NOCs) and their disturbances in the environment. This thesis is aimed on assessment of levels and trends of naturally produced brominated compounds in Baltic biota; more specifically on hydroxylated polybrominated diphenyl ethers (OH-PBDEs), methoxylated PBDEs (MeO-PBDEs) and polybrominated dibenzo-p-dioxins (PBDDs). These, NOCs, may originate from production in algae and cyanobacteria. OH-PBDEs and MeO-PBDEs may also be formed as metabolites of polybrominated diphenyl ethers (PBDEs), i.e. well-known commercial flame retardants. High levels of OH-PBDEs, MeO-PBDEs and PBDDs are shown within Baltic biota (cyanobacteria, algae, mussels, fish), often in much higher concentrations than PBDEs which are possible anthropogenic precursors of OH- and MeO-PBDEs. The levels of OH-PBDEs, MeO-PBDEs and PBDDs are higher in the Baltic Sea than on the west coast of Sweden. Temporal and seasonal variations show fluctuations in concentrations of OH-PBDEs, MeO-PBDEs and PBDDs, possibly related with macroalgal life-cycles. OH-PBDEs, MeO-PBDEs and PBDDs are present in several filamentous macroalgae species, but considering the levels quantified, the time of peak exposure and the species life-cycle the macroalgae, Pilayella, Ceramium and Cladophora are suggested as major natural producers of OH-PBDEs and PBDDs. The high levels of OH-PBDEs, MeO-PBDEs and PBDDs in the Baltic Sea may affect numerous organisms in the ecosystem. The toxic effects of OH-PBDEs and PBDDs are of particular concern. This thesis stress the importance of assessing and monitoring these substances, since the exposure to OH-PBDEs and PBDDs, during summer, may cause acute effects in Baltic fish and wildlife.
At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: In press. Paper 4: Manuscript.
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Ortuño, García Nuria. "Descomposición térmica de residuos de aparatos eléctricos y electrónicos: estudio cinético y formación de contaminantes." Doctoral thesis, Universidad de Alicante, 2014. http://hdl.handle.net/10045/41605.

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Hroch, Martin. "Studium distribuce halogenovaných difenyletherů do složek životního prostředí." Doctoral thesis, Vysoké učení technické v Brně. Fakulta chemická, 2012. http://www.nusl.cz/ntk/nusl-233346.

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In recent years considerable attention is paid to problems of brominated flame retardants (BFR's – Brominated Flame retardants), which are a diverse group of organic compounds. Even in the recent past have been the most often represented group particularly polybrominated diphenyl ethers (PBDEs), which have found wide use in many industrial sectors. The reason of aplication of these substances is the ability to slow down the combustion process and reduce the risk of ignition by the excessive heating of material. On the other hand, serious concerns about the use of PBDEs was added. The most serious trouble is particular their possible to release from consumer products during their normal use, toxicity and high persistence in parts of environment. Some of these contaminants are more characterized by a high degree of accumulation in biological systems. In this work by several sub-studies the issue of assessment the level of pollution of the aquatic ecosystem of selected localities of the Czech Republic just PBDEs was addressed. One of objectives was monitored the situation of breeding ponds near the village Záhlinice in Central Moravia. Here was assessed level of contamination in fish and birds as two consecutive segments of food chain. The obtained results largely confirmed the assumption that with increasing trophic level of organisms leads to bioaccumulation and thus also higher findings. For comparison, the capture of fish and birds in other localities of the CR was also implemented. In Bartošovice and Hustopeče nad Becvou levels at the buzzard and heron were detected as comparable. The cormorants of the order higher levels of PBDEs were found. Further were also evaluated levels of PBDEs detected in individuals of bioindicator kind of chub caught in two locations on the river Svratka in spring and autumn. Findings of PBDE in muscle, skin and intestines were compared. The obtained results show that between tissues and sites wasn’t significant variability respectively and the findings of controlled substances are practically comparable. With aim to determine the dependence of the concentration of PBDEs in organisms on the length of the river was conducted monitoring of Vír and Brno water reservoirs. In both locations was main monitored kind of bream, which was completed by the other species. The results of the analysis indicate a higher total concentration at the lower part of river Svratka. Differences were also the distribution of individual congeners in both sampling locations. For monitoring of terrestrial system contamination levels of PBDEs has been selected several types of plant bioindicators. These are mainly pine needles (Scots pine, Eastern white pine, Silver fir, Blue spruce) collected from different localities of the Czech Republic. Other matrices were chosen roughages (Common wheat, Naked barley, Alfalfa wheat, Red clover) and oilseeds (Rapeseed) from the Novy Jicin, where Agriculture plant school of the University of Veterinary and Pharmaceutical Sciences Brno. Detected values of PBDE concentrations were very low, generally ranged at the detection limits of the analytical method.
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Khan, Simeen. "Colloidal PbS and PbS/CdS Core/Shell Nanosheets." Bowling Green State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1447955111.

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Books on the topic "PBDs"

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Public Broadcasting Service (U.S.), ed. PBS previews 2003. [Alexandria, Va.]: PBS, 2002.

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Demokrat, Partai Buruh Sosial. Partai Buruh Sosial Demokrat: PBSD. 2nd ed. Jakarta: DPP PBSD, 2001.

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R, Shulman Shelia, Healy Elaine M, and Lasagna Louis 1923-, eds. PBMs: Reshaping the pharmaceutical distribution network. New York: Pharmaceutical Products Press, 1998.

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1942-, Coover Edwin R., ed. Tutorial, digital private branch exchanges (PBXs). Washington, D.C: IEEE Computer Society Press, 1989.

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Kids, PBS for. PBS kids: Dragonfly TV. [Alexandria, VA]: PBS, 2003.

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Talib, Khusairie. PBS keluar membela maruah. Kuala Lumpur: Goldana Corp., 1991.

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Online, PBS, and Democracy Project (Public Broadcasting Service), eds. The PBS democracy project. [Alexandria, Va.?]: PBS Online, 2000.

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Jarvik, Laurence Ariel. PBS, behind the screen. Rocklin, CA: Forum, 1997.

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Crocker, Mel. Black cats and dumbos: WWII's fighting PBYs. Blue Ridge Summit, PA: AERO, 1987.

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Crocker, Mel. Black cats and dumbos: WWII's fighting PBYs. 2nd ed. Huntington Beach, CA: Crocker Media Expressions, 2002.

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Book chapters on the topic "PBDs"

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GÄrtner, Jutta. "Is there a Phenotype/Genotype Correlation in Peroxisome Biogenesis Disorders (PBDs)?" In Advances in Experimental Medicine and Biology, 59–65. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9072-3_7.

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Gooch, Jan W. "PBS." In Encyclopedic Dictionary of Polymers, 521. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_8479.

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Hilmes, Michele. "PBS." In From Networks to Netflix, 55–65. New York : Routledge, 2018.: Routledge, 2018. http://dx.doi.org/10.4324/9781315658643-5.

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Hilmes, Michele. "PBS." In From Networks to Netflix, 47–58. 2nd ed. New York: Routledge, 2022. http://dx.doi.org/10.4324/9781003099499-6.

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Hollins-Sims, Nikole Y., Erica J. Kaurudar, and Timothy J. Runge. "Setting the Foundation." In Creating Equitable Practices in PBIS, 1–20. New York: Eye on Education, 2022. http://dx.doi.org/10.4324/9781003294351-1.

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Hollins-Sims, Nikole Y., Erica J. Kaurudar, and Timothy J. Runge. "Where Do We Go From Here?" In Creating Equitable Practices in PBIS, 129–52. New York: Eye on Education, 2022. http://dx.doi.org/10.4324/9781003294351-5.

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Hollins-Sims, Nikole Y., Erica J. Kaurudar, and Timothy J. Runge. "Implementation and Evaluation." In Creating Equitable Practices in PBIS, 60–94. New York: Eye on Education, 2022. http://dx.doi.org/10.4324/9781003294351-3.

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Hollins-Sims, Nikole Y., Erica J. Kaurudar, and Timothy J. Runge. "Data Rich & Information Rich." In Creating Equitable Practices in PBIS, 95–128. New York: Eye on Education, 2022. http://dx.doi.org/10.4324/9781003294351-4.

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Hollins-Sims, Nikole Y., Erica J. Kaurudar, and Timothy J. Runge. "Beginning the Journey." In Creating Equitable Practices in PBIS, 21–59. New York: Eye on Education, 2022. http://dx.doi.org/10.4324/9781003294351-2.

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Schneider, Tobias. "Methodische Grundlagen eines PBRS." In Preference-Based-Recommender-Systeme, 27–116. Wiesbaden: Deutscher Universitätsverlag, 2005. http://dx.doi.org/10.1007/978-3-322-81959-8_3.

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Conference papers on the topic "PBDs"

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Jackson, Paul J. M., George Procopiou, Nicolas Veillard, Julia Mantaj, K. Miraz Rahman, and David E. Thurston. "Abstract 4779: In silico design, synthesis and evaluation of a new family of C1-substituted pyrrolobenzodiazepines (PBDs)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4779.

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Vlahov, Iontcho, Albert Felten, Ning Zou, Kevin Wang, Hari K. Santhapuram, Paul Kleindl, Spencer Hahn, Jeremy Vaughn, and Christopher Leamon. "Abstract 757: Novel warheads for targeted therapies of cancer: The concept and design of oxime-ether-based pro-PBDs." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-757.

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Hua, L., Y. P. Wu, B. An, Y. C. Chan, B. Y. Wu, and F. S. Wu. "The Determinations of Pb, Cd, Hg, Cr6+, PBBs/PBDEs to Comply with RoHS Directive." In 2007 8th International Conference on Electronic Packaging Technology. IEEE, 2007. http://dx.doi.org/10.1109/icept.2007.4441478.

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Xie, Liang, Xinwen Zhang, Jean-Pierre Seifert, and Sencun Zhu. "pBMDS." In the third ACM conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1741866.1741874.

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Bobba, Rakesh, Himanshu Khurana, Musab AlTurki, and Farhana Ashraf. "PBES." In the 4th International Symposium. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1533057.1533093.

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Zhao, Juan, Junqiang Song, Min Zhu, Jincai Li, Zhenyu Huang, Xiaoyong Li, and Xiaoli Ren. "PBCS." In ICPP 2018: 47th International Conference on Parallel Processing. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3225058.3225097.

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Zhang, Xinwen, Sejong Oh, and Ravi Sandhu. "PBDM." In the eighth ACM symposium. New York, New York, USA: ACM Press, 2003. http://dx.doi.org/10.1145/775412.775431.

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Feng, Hanhua, Vishal Misra, and Dan Rubenstein. "PBS." In the 2007 ACM SIGMETRICS international conference. New York, New York, USA: ACM Press, 2007. http://dx.doi.org/10.1145/1254882.1254906.

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Nave, Eyal Itzhak, and Ran Ginosar. "PBD." In the 23rd ACM international conference. New York, New York, USA: ACM Press, 2013. http://dx.doi.org/10.1145/2483028.2483121.

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Humphrey, Michael. "Altair's PBS---Altair's PBS professional update." In the 2006 ACM/IEEE conference. New York, New York, USA: ACM Press, 2006. http://dx.doi.org/10.1145/1188455.1188484.

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Reports on the topic "PBDs"

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Dickson, Peter, Gary Robert Parker, and Philip John Rae. The Thermal Response of TATB-Based PBXs. Office of Scientific and Technical Information (OSTI), January 2015. http://dx.doi.org/10.2172/1168714.

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Freye, Christopher. Gel Permeation Chromatography Methods for Stockpile Relevant PBXs. Office of Scientific and Technical Information (OSTI), November 2021. http://dx.doi.org/10.2172/1828703.

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Widmayer, C., and K. Manes. NIF-0096141-OA Prop Simulations of NEL PBRS Measurements. Office of Scientific and Technical Information (OSTI), February 2003. http://dx.doi.org/10.2172/15005257.

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Góngora, Pamela, and Úrsula Giedion. Breve 26. Diseño y costeo de un Plan de Beneficios en Salud en un país de ingreso medio-bajo: el caso de Honduras. Banco Interamericano de Desarrollo, June 2022. http://dx.doi.org/10.18235/0004317.

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Honduras es un país de ingresos medios bajos con un sistema de salud fragmentado y menos de US$100 per cápita por año para satisfacer sus necesidades de salud. En el marco de su compromiso por la Cobertura Universal de Salud (CUS), el gobierno decidió diseñar un Plan de Beneficios en Salud (PBS). El diseño del PBS se realizó en cinco pasos. (1) Un equipo interinstitucional del Ministerio de Salud de Honduras y del Instituto de Seguridad Social definió las características fundamentales del PBS. (2) Aprovechando trabajos previos realizados en el país, se identificó el universo de los potenciales candidatos a inclusión. (3) Se discutieron y operacionalizaron criterios de priorización y reglas de decisión. (4) Se utilizó un enfoque ascendente para costear el PBS, con la baja cobertura actual y con diferentes objetivos de mejora de los niveles de cobertura. (5) Se elaboraron análisis de impacto fiscal y se discutieron caminos alternativos de expansión con el gobierno planteando criterios éticos en el camino hacia la CUS. El PBS resultante incluye 74 intervenciones esenciales de salud. Dadas las restricciones financieras, se sugirió un camino de expansión progresiva, mediante el cual los aumentos marginales en el presupuesto de salud se asignarían al PBS. El diseño de un PBS es un proceso específico a cada contexto; incluye varios pasos que van más allá de la implementación de métodos de evaluación de tecnologías sanitarias y requiere mucho tiempo de trabajo técnico y participativo y un pragmatismo sustancial para adaptar las recomendaciones técnicas de la literatura a los datos y a las restricciones de tiempo sobre el terreno.
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Forsberg, Charles W., and David Lewis Moses. Safeguards Challenges for Pebble-Bed Reactors (PBRs):Peoples Republic of China (PRC). Office of Scientific and Technical Information (OSTI), November 2009. http://dx.doi.org/10.2172/969660.

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Stapleton, Heather M., Jennifer M. Keller, Michele M. Schantz, John R. Kucklick, and Stephen A. Wise. NIST inter-comparison exercise program for polybrominated diphenyl ethers (PBDEs) in marine sediment:. Gaithersburg, MD: National Institute of Standards and Technology, 2005. http://dx.doi.org/10.6028/nist.ir.7278.

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Velizhanin, Kirill A. Enhanced Multiple Exciton Generation in PbS|CdS Janus-like Heterostructured Nanocrystals. Office of Scientific and Technical Information (OSTI), March 2019. http://dx.doi.org/10.2172/1498021.

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White, C. W., J. D. Budai, and A. L. Meldrum. Ion beam synthesis of CdS, ZnS, and PbS compound semiconductor nanocrystals. Office of Scientific and Technical Information (OSTI), December 1997. http://dx.doi.org/10.2172/564245.

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Michael, Thad J. Evaluation and Improvement of the PBD-X/MTFLOW Propulsor Analysis Software. Fort Belvoir, VA: Defense Technical Information Center, December 2009. http://dx.doi.org/10.21236/ada512363.

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Dereviankin, Vitalii. Development of a Liquid Contacting Method for Investigating Photovoltaic Properties of PbS Quantum Dot Solids. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6124.

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