The use of telehealth in healthcare has grown in recent years; however, little is known about the effectiveness of this delivery method in the management of Type 2 diabetes mellitus (T2DM). Guided by the chronic care model and telehealth in chronic disease model, the purpose of this systematic literature review was to explore evidence related to lowering hemoglobin A1c levels and managing T2DM using telehealth in the outpatient setting. The practice-focused questions explored telehealth interventions used in T2DM management and their effectiveness. The Joanna Briggs Institute (JBI) method for conducting systematic literature reviews was the process, and data were compiled using the PRISMA evidence-based minimum set for reporting. Eighteen studies met the inclusion criteria for this project. Data were extracted, analyzed, and synthesized using JBI tools for data extraction and critical appraisal. Article appraisals revealed numerous telehealth interventions for management of T2DM including telephone, Internet-based, clinical video, remote monitoring, and smart phones/applications. Overall, telehealth interventions showed statistically significant improvement in the hemoglobin A1c levels of participants compared to traditional outpatient care. Success of the interventions is associated with components of evidenced-based diabetes management such as education, self-management, support, and feedback loop. The implications of this project for positive social change include the integration of telehealth interventions in the outpatient setting to manage T2DM with enhanced access to care, reduction in health disparities, and improved health outcomes for society.

Vitamin A deficiency (VAD) affects 12% of Peruvians under 5 years of age. Recent studies have shown an association with hematopoiesis and iron metabolism. In Peru, 3-quarters of a million children have anemia. We aimed to identify an association between Vitamin A supplementation (VAS) and anemia in children under 5 years of age. A cross-sectional secondary analytical study from the Peruvian Demographic Survey and Family Health (DHS) was conducted. The primary outcome, anemia, was measured through hemoglobin concentration and adjusted by altitude. The DHS interviewer ensured the participant’s VAS in the last 6 months through a structural healthcare card. The association was statistically significant using crude regression but disappeared when adjusted per socioeconomic level and gender. VAS was not significantly associated with a lower prevalence of anemia. Further studies are required to help identify the association between VAS and anemia. / Revisión por pares

In humans, washing stored blood products prior to transfusion reduces storage lesions and the potential for transfusion reaction, but the effectiveness of washing units of canine whole blood is unknown. The objective of this study was to determine if a manual method of washing of stored whole blood units reduced storage lesions without adversely affecting erythrocytes. Units of canine whole blood were stored for 28 days and manually washed three times with sterile .9% NaCl. Following the first wash, there was a decrease in serum potassium (P<.0001), lactate (P<.0001), pH (P=.0110), pCO2 (P<.0001), TCO2 (P<.0001), arachidonic acid (P<.0001), and thromboxane B2 (P=.0417), and increases in iCa (P=.0494), iMg (P=.0024), MCV (P<.0001), MCHC (P=.0093), RDW (P=.0009), hemoglobin (P=.0011), and MCF (P=.0006). No bacterial growth was identified on the post-transfusion samples. Manual washing of stored blood significantly reduces storage lesions after a single wash and additional washing may cause in vitro hemolysis.

Analysis of hemogobins were conducted on animals of the species Ambystoma tigrinum. Separation of hemoglobin types was performed with a Carboxy-methyl-cellulose column (6 X 50 mm.) and pH gradient (pH 6 thru 8) of .01 M phosphate buffer. The hemoglobins in the effluent were detected and analysed with a micro-flow cell in a Beck-man DB-G spectrophotometer attached to a Photovolt Varicord 43 recorder. Two major components of hemoglobin were observed: larval and adult. These two components varied in concentration with the stage of development of the individual. In addition, it was noted that minor peaks ansd shoulders appeared on each peak wich were consistant and characteristic for each major hemoglobin type.

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Zhang, Siwei. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 87-98). / Abstracts in English and Chinese. / Chapter 1. --- General introduction --- p.1 / Chapter 1.1. --- "Types, structure and function of human hemoglobin" --- p.1 / Chapter 1.1.1. --- Structure and functions of human hemoglobin --- p.1 / Chapter 1.1.2. --- Types of human hemoglobin --- p.2 / Chapter 1.2. --- Regulatory mechanism of human hemoglobin expression --- p.3 / Chapter 1.2.1. --- The human a and β locus --- p.3 / Chapter 1.2.2. --- Development of globin genes switching concept --- p.4 / Chapter 1.2.3. --- Factors that regulate globin gene expression --- p.5 / Chapter 1.2.3.1. --- The locus control region (LCR) --- p.5 / Chapter 1.2.3.2. --- The cis-regulatory elements --- p.5 / Chapter 1.2.3.3. --- The trans-acting factors --- p.6 / Chapter 1.3. --- The human hemoglobinopathies --- p.8 / Chapter 1.3.1. --- α-thalassemia --- p.8 / Chapter 1.3.2. --- β-thalassemia --- p.9 / Chapter 1.3.3. --- Sickle cell anemia --- p.10 / Chapter 1.4. --- Current approaches towards β-thalassemia treatment --- p.11 / Chapter 1.4.1. --- Blood transfusion --- p.11 / Chapter 1.4.2. --- Bone marrow transplantation --- p.12 / Chapter 1.4.3. --- Drug-induced activation of fetal hemoglobin production --- p.12 / Chapter 1.4.3.1. --- Hydroxyurea --- p.12 / Chapter 1.4.3.2. --- Butyrate and short-chain fatty acids --- p.13 / Chapter 1.4.3.3. --- "Mutagens, DNA methyltransferase inhibitors and other HbF inducible agents" --- p.13 / Chapter 1.4.3.4. --- Cucurbitacin D --- p.14 / Chapter 1.4.4. --- Gene therapy --- p.14 / Chapter 1.5. --- Research Objectives --- p.15 / Chapter 2. --- "Analysis of CuD, Hydroxyurea and other inducers on the induction of α, β, γ, δ， ε，ζ BP-1 genes and fetal hemoglobin induction" --- p.16 / Chapter 2.1. --- Introduction --- p.16 / Chapter 2.1.1. --- Properties of human K562 cell line --- p.16 / Chapter 2.1.2. --- Induction and measurement of fetal hemoglobin --- p.16 / Chapter 2.1.3. --- "Induction of α, β, γ, δ, ε , ζ and BP-1 gene and Real-time RT-PCR analysis" --- p.17 / Chapter 2.2. --- Materials --- p.18 / Chapter 2.2.1. --- Chemicals and reagents --- p.18 / Chapter 2.2.2. --- Kits --- p.19 / Chapter 2.2.3. --- Buffers and solutions --- p.19 / Chapter 2.2.4. --- Cell lines --- p.20 / Chapter 2.3. --- Experimental procedures --- p.20 / Chapter 2.3.1. --- Hemoglobin quantity measurement by HbF ELISA --- p.20 / Chapter 2.3.1.1. --- MTT assay --- p.21 / Chapter 2.3.1.2. --- Preparation of capture-antibody coated ELISA plates --- p.21 / Chapter 2.3.1.3. --- Plate blocking --- p.22 / Chapter 2.3.1.4. --- Sample and standard preparation --- p.22 / Chapter 2.3.1.5. --- HRP antibody and colorimetric detection --- p.23 / Chapter 2.3.1.6. --- Statistical analysis --- p.23 / Chapter 2.3.2. --- Preparation of mRNA extract from K562 cells --- p.23 / Chapter 2.3.3. --- Reverse transcription and Real-time PCR analysis --- p.24 / Chapter 2.4. --- Results --- p.25 / Chapter 2.4.1. --- CuD significantly upregulates HbF expression in K562 cells --- p.25 / Chapter 2.4.2. --- "CuD augments α, β, γ, δ, ε , ζ and BP-1 genes at different level in K562 cells" --- p.28 / Chapter 2.4.3. --- Cucurbitacin D-induced γ-globin gene activation requires12-24 hours in K562 cells --- p.31 / Chapter 2.5. --- Discussion --- p.33 / Chapter 2.5.1. --- Enhancement of fetal hemoglobin production using different chemical compounds --- p.33 / Chapter 2.5.2. --- CuD increased HbF synthesis by increasing γ-globin mRNA amount --- p.35 / Chapter 2.5.3. --- CuD and HU down-regulated the BP-1 gene expression --- p.36 / Chapter 3. --- Determination of potential signal transduction pathways during CuD and HU-mediated fetal hemoglobin production --- p.36 / Chapter 3.1. --- Introductions --- p.36 / Chapter 3.1.1. --- The p38 MAPK family --- p.37 / Chapter 3.1.2. --- The JAK2-STAT3 pathway --- p.38 / Chapter 3.1.3. --- Fundamentals on inhibition assay of p38 MAPK and JAK2-STAT3 pathway --- p.39 / Chapter 3.1.4. --- Fundamentals on nuclear translocation of STAT3 --- p.41 / Chapter 3.2. --- Materials --- p.41 / Chapter 3.2.1. --- Chemicals and reagents --- p.41 / Chapter 3.2.2. --- Kits --- p.44 / Chapter 3.2.3. --- Buffers and solutions --- p.44 / Chapter 3.3. --- Experimental procedures --- p.45 / Chapter 3.3.1. --- Detection of p3 8 MAPK phosphorylation status --- p.46 / Chapter 3.3.1.1. --- Preparation of cytosolic protein extracts --- p.46 / Chapter 3.3.1.2. --- Quantitative measurement of phospho-p38 and pan-p38 by ELIS A method --- p.46 / Chapter 3.3.1.2.1. --- Antigen adsorption and establishment of standard curves --- p.46 / Chapter 3.3.1.2.2. --- Plate washing and application of detection antibody --- p.47 / Chapter 3.3.1.2.3. --- Plate washing and application of secondary antibody --- p.47 / Chapter 3.3.1.2.4. --- Plate washing and chromogen detection --- p.48 / Chapter 3.3.2. --- Detection of signal cascade on JAK2-STAT3 pathway --- p.48 / Chapter 3.3.2.1. --- Preparation of cytosolic protein extracts for Western Blot detection --- p.48 / Chapter 3.3.2.2. --- Gel running and Western Blot detection --- p.48 / Chapter 3.3.3. --- Quantitative measurement of phospho-STAT3-Tyr705 using ELISA method --- p.50 / Chapter 3.3.3.1. --- Preparation of cytosolic protein extracts --- p.50 / Chapter 3.3.3.2. --- Reconstitution and Dilution of STAT3 [pY705] Standard --- p.50 / Chapter 3.3.3.3. --- Measurement of STAT3 [pY705] concentration in cell lysates --- p.51 / Chapter 3.3.4. --- Inhibitor assay of JAK2-STAT3 and p38 MAPK pathway --- p.52 / Chapter 3.3.4.1. --- Establishment of inhibitor assay --- p.52 / Chapter 3.3.4.2. --- HbF ELISA detection --- p.53 / Chapter 3.3.5. --- Detection of STAT3 nuclear translocation and DNA binding affinity --- p.53 / Chapter 3.3.5.1. --- Preparation of nuclear extract from K562 cells --- p.53 / Chapter 3.3.5.2. --- EMS A detection of transcriptional factors binding to γ-promoter region --- p.54 / Chapter 3.3.5.2.1. --- 3´ة end-labeling of EMS A probes --- p.54 / Chapter 3.3.5.2.2. --- Dot blotting for labeling efficiency estimation --- p.56 / Chapter 3.3.5.2.3. --- EMSA binding reaction and non-denaturing gel electrophoresis --- p.57 / Chapter 3.3.5.2.4. --- Membrane development and chemiluminescence detection --- p.58 / Chapter 3.3.5.3. --- Preparation of K562 samples for immunofluorescence detection --- p.60 / Chapter 3.3.5.3.1. --- Slide coating for cell capture --- p.60 / Chapter 3.3.5.3.2. --- Preparation of cell slide --- p.60 / Chapter 3.3.5.3.3. --- Sample fixation and antibody probing treatment --- p.60 / Chapter 3.3.5.3.4. --- Sample imaging and immunofluorescence detection --- p.61 / Chapter 3.4 --- Results --- p.62 / Chapter 3.4.1. --- Activation of p38 MAPK pathway and STAT3 phosphorylation by hydroxyurea --- p.62 / Chapter 3.4.1.1. --- "The p38 MAPK pathway is activated by hydroxyurea, but not activated by Cucurbitacin D" --- p.62 / Chapter 3.4.1.2. --- Increased p38 phosphorylation level elicits STAT3 phosphorylation at Ser727 site --- p.64 / Chapter 3.4.2. --- Activation of JAK2 and STAT3 phosphorylation by Cucurbitacin D --- p.66 / Chapter 3.4.2.1. --- Cucurbitacin D promotes JAK2 activation --- p.66 / Chapter 3.4.2.2. --- Cucurbitacin D and hydroxyurea promote STAT3 phosphorylation at Tyr705 site --- p.66 / Chapter 3.4.3. --- Basal activity of signal transduction pathways is essential for HbF induction --- p.69 / Chapter 3.4.3.1. --- Activation of γ-globin gene requires presence of basal phosphorylation level of p38 MAPK --- p.69 / Chapter 3.4.3.2. --- Inhibition on JAK2-STAT3 pathway results in reduced fetal hemoglobin production --- p.71 / Chapter 3.4.4. --- Translocation and DNA binding of STAT under Cucurbitacin D induction --- p.72 / Chapter 3.4.4.1. --- Cucurbitacin D and hydroxyurea both enhance binding affinity of transcriptional factors to the Gγ/Aγ promoter --- p.72 / Chapter 3.4.4.2. --- Cucurbitacin D and hydroxyurea induces nuclear translocation of STAT3 --- p.75 / Chapter 3.5. --- Discussion --- p.77 / Chapter 3.5.1. --- The role of p38 MAPK activation during γ-globin gene activation --- p.77 / Chapter 3.5.2. --- STAT3 phosphorylation at Ser727 site promotes transcription factor activity and γ-globin gene expression --- p.77 / Chapter 3.5.3. --- The role of JAK2-STAT3 activation during γ-globin gene activation --- p.78 / Chapter 3.5.4. --- Inhibitor assay --- p.79 / Chapter 3.5.5. --- Relations between STAT3 nuclear translocation and enhanced fetal hemoglobin production --- p.82 / Chapter 4. --- Summery and Prospect --- p.83 / Chapter 5. --- References --- p.87

Daug pasaulinių organizacijų, kurios stengiasi pagerinti cukrinio diabeto diagnostiką ir sergančių pacientų glikemijos kontrolę, nes nepakankama ir vėlyva diagnostika skatina komplikacijų atsiradimą ir progresavimą. Šio darbo tikslas išanalizuoti cukriniu diabetu sergančių pacientų metodologinių ypatumų įtaką glikozilinto hemoglobino rezultatams. Išmatavus analitę HbA1c, 100 pacientų sergančių cukriniu diabetu, trimis skirtingos standartizacijos analizinėmis sistemomis Roche-Hitachi 917, Bayer-Advia1650 ir Dade Behring-Dimension RxL, gauta koreliacija su trijų mėnesių gliukozės koncentracijos vidurkiu. Lyginant HbA1c rezultatus, referentiniu metodu Roche-Hitachi 917 analizine sistema, standartizuota Tarptautinės klinikinės chemijos ir laboratorinės medicinos federacijos (IFCC) ir Diabeto kontrolės ir komplikacijų tyrimų (DCCT), gautas skirtumas. Bayer-Advia1650 analizinė sistema, kurios HbA1c metodas standartizuotas Nacionalinės glikohemoglobino standartizacijos programos (NGSP), lyginant su mūsų referentinio metodo rezultatais, kai IFCC standartizacija r = 1.017 [0.883 iki 1.188]; y = 3.068 [1.894 iki 4.142]; n = 52; p = 0.0000001, o kai standartizacija DCCT r = 1.132 [1.060 iki 1.209]; y = 0.282 [-0.476 iki 0.990]; n = 53; p = 0.001. Dade Behring-Dimension RxL analizinės sistemos metodas standartizuotas pagal Diabeto kontrolės ir komplikacijų tyrimus (DCCT) palyginus su IFCC standartizuotu metodu rezultatais: r = 0.886 [0.767 iki 1.021]; y = 2.422 [1.630 iki 3.413]; n = 52... [toliau žr. visą tekstą] / There are many organisations trying to improve Diabetes Mellitus diagnostics, enhance glycaemia management of diabetes patients, because insufficient and late diagnosis increases formation, and complications progress. The purpose of this work was evolution of influence, of different methodological approaches to of glycated hemoglobin results. Samples of 100 patients with Diabetes Mellitus was analyzed for glucose and HbA1c. There was shown correlation between average concentration glucose‘s during three months coefficient. HbA1c was analyzed using three analytical systems of Roche-Hitachi 917, Bayer-Advia1650 and Dade Behring-Dimension RxL standardized according different standardization recommendations: International Federation of Clinical Chemistry and Laboratory Medicine (IFCC), Diabetes Control and Complications Trial (DCCT), National Glycohemoglobin Standardization Program (NGSP). Roche-Hitachi 917 results standardized according IFCC recommendations were chosen as reference. Correlation and differences between analytical systems were as follows. Roche-Hitachi 917 (IFCC) – Bayer-Advia1650 (NGSP): r = 1.017 [0.883 to 1.188]; y = 3.068 [1.894 to 4.142]; n = 52; p = 0.0000001. Roche-Hitachi 917 (DCCT) – Bayer-Advia1650 (NGSP): r = 1.132 [1.060 to 1.209]; y = 0.282 [-0.476 to 0.990]; n = 53; p = 0.001. Roche-Hitachi 917 (IFCC) – Dade Behring-Dimension RxL (DCCT): 0.886 [0.767 to 1.021]; y = 2.422 [1.630 to 3.413]; n = 52; p = 0.0000001. Roche-Hitachi 917 (DCCT) – Dade... [to full text]

Thesis (Ph.D.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 121 pages. Includes Vita. Includes bibliographical references.

Thesis (Ph.D.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 125 pages. Includes Vita. Includes bibliographical references.