XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Standards of Medical Care in Diabetes

AMP-activated protein kinase (AMPK) is a crucial cellular energy sensor. Once activated by falling energy status, it promotes ATP production by increasing the activity or expression of proteins involved in catabolism while conserving ATP by switching off biosynthetic pathways. AMPK also regulates metabolic energy balance at the whole-body level. For example, it mediates the effects of agents acting on the hypothalamus that promote feeding and entrains circadian rhythms of metabolism and feeding behaviour. Finally, recent studies reveal that AMPK conserves ATP levels through the regulation of processes other than metabolism, such as the cell cycle and neuronal membrane excitability.

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AMPK: a nutrient and energy sensor that maintains energy homeostasis

I read this book the same weekend that the Packers took on the Rams, and the experience of the latter event, obviously, colored my judgment. Although I abhor anything that smacks of being a handbook (like, \"How to Earn a Merit Badge in Neurosurgery\") because too many volumes in biomedical science already evince a boyscout-like approach, I must confess that parts of this volume are fast, scholarly, and significant, with certain reservations. I like parts of this well-illustrated book because Dr. Sj6strand, without so stating, develops certain subjects on technique in relation to the acquisition of judgment and sophistication. And this is important! So, given that the author (like all of us) is somewhat deficient in some areas, and biased in others, the book is still valuable if the uninitiated reader swallows it in a general fashion, realizing full well that what will be required from the reader is a modulation to fit his vision, propreception, adaptation and response, and the kind of problem he is undertaking. A major deficiency of this book is revealed by comparison of its use of physics and of chemistry to provide understanding and background for the application of high resolution electron microscopy to problems in biology. Since the volume is keyed to high resolution electron microscopy, which is a sophisticated form of structural analysis, but really morphology in a modern guise, the physical and mechanical background of The instrument and its ancillary tools are simply and well presented. The potential use of chemical or cytochemical information as it relates to biological fine structure , however, is quite deficient. I wonder when even sophisticated morphol-ogists will consider fixation a reaction and not a technique; only then will the fundamentals become self-evident and predictable and this sine qua flon will become less mystical. Staining reactions (the most inadequate chapter) ought to be something more than a technique to selectively enhance contrast of morphological elements; it ought to give the structural addresses of some of the chemical residents of cell components. Is it pertinent that auto-radiography gets singled out for more complete coverage than other significant aspects of cytochemistry by a high resolution microscopist, when it has a built-in minimal error of 1,000 A in standard practice? I don't mean to blind-side (in strict football terminology) Dr. Sj6strand's efforts for what is \"routinely used in our laboratory\"; what is done is usually well done. It's just that …

Methods in Enzymology.

The TRIPOD (Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis) Statement includes a 22-item checklist, which aims to improve the reporting of studies developing, validating, or updating a prediction model, whether for diagnostic or prognostic purposes. The TRIPOD Statement aims to improve the transparency of the reporting of a prediction model study regardless of the study methods used. This explanation and elaboration document describes the rationale; clarifies the meaning of each item; and discusses why transparent reporting is important, with a view to assessing risk of bias and clinical usefulness of the prediction model. Each checklist item of the TRIPOD Statement is explained in detail and accompanied by published examples of good reporting. The document also provides a valuable reference of issues to consider when designing, conducting, and analyzing prediction model studies. To aid the editorial process and help peer reviewers and, ultimately, readers and systematic reviewers of prediction model studies, it is recommended that authors include a completed checklist in their submission. The TRIPOD checklist can also be downloaded from www.tripod-statement.org.

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Transparent Reporting of a multivariable prediction model for Individual Prognosis or Diagnosis (TRIPOD): explanation and elaboration.

Non-thrombotic PE does not represent a distinct clinical syndrome. It may be due to a variety of embolic materials and result in a wide spectrum of clinical presentations, making the diagnosis difficult. With the exception of severe air and fat embolism, the haemodynamic consequences of non-thrombotic emboli are usually mild. Treatment is mostly supportive but may differ according to the type of embolic material and clinical severity.

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Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)

Molecular cloning of fatty acid-transport protein cDNA from rat.

In view of the importance of long chain fatty acids (LCFAs) to many cellular processes, it may be desirable to regulate the LCFA disposition in the cell. Such regulation may be present at the level...

Fatty acid transport proteins facilitate fatty acid uptake in skeletal muscle.

Lipids serve a great variety of functions, ranging from structural components of biological membranes to signaling molecules affecting various cellular functions. Several of these functions are related to the unique physico-chemical properties shared by all lipid species, i.e., their hydrophobicity. The latter, however, is accompanied by a poor solubility in an aqueous environment and thus a severe limitation in the transport of lipids in aqueous compartments such as blood plasma and the cellular soluble cytoplasm. Specific proteins which can reversibly and non-covalently associate with lipids, designated as lipid binding proteins or lipid chaperones, greatly enhance the aqueous solubility of lipids and facilitate their transport between tissues and within tissue cells. Importantly, transport of lipids across biological membranes also is facilitated by specific (membrane-associated) lipid binding proteins. Together, these lipid binding proteins determine the bio-availability of their ligands, and thereby markedly influence the subsequent processing, utilization, or signaling effect of lipids. The bio-availability of specific lipid species thus is governed by the presence of specific lipid binding proteins, the affinity of these proteins for distinct lipid species, and the presence of competing ligands (including pharmaceutical compounds). Recent studies suggest that post-translational modifications of lipid binding proteins may have great impact on lipid-protein interactions. As a result, several levels of regulation exist that together determine the bio-availability of lipid species. This short review discusses the significance of lipid binding proteins and their potential application as targets for therapeutic intervention.

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Lipids and lipid binding proteins: a perfect match.

Amperometric enzyme immunosensors have been developed for the detection of the early myocardial infarction marker heart fatty acid binding protein (H-FABP) in blood plasma. They are based on anti-H-FABP antibodies immobilized on nitrocellulose or activated nylon membranes covering a modified Clark-type oxygen electrode. Two approaches have been tested using bovine H-FABP as a model: (i) the competition principle, where defined amounts of glucose oxidase (GOD)-labelled H-FABP compete with free H-FABP for binding to the immobilized capture antibodies; (ii) the sandwich principle, where the free H-FABP binds to the immobilized capture antibody and to a secondary GOD-labelled antibody, forming a sandwich. In both approaches, after addition of glucose, the activity of the enzyme label is determined with the amperometric electrode within minutes. The immunosensor using the sandwich principle on activated nylon membranes can be used repeatedly for at least 10 measurements after regeneration of the antibody membranes without loss of binding capacity of the capture antibodies. For the determination of human H-FABP, the sandwich principle with monoclonal anti-bovine-H-FABP antibodies as capture and GOD-labelled goat-anti-human-H-FABP antibodies as secondary antibodies is chosen. Initial experiments demonstrate that the sensitivity of the immunosensor is sufficient for the determination of clinical levels of H-FABP in plasma after myocardial infarction (100–300 ng ml−1).

Enzyme immunosensor for diagnosis of myocardial infarction

Heart-type fatty acid-binding protein (FABP; M r 14 500) is an early plasma marker of acute myocardial infarction (AMI) (1)(2)(3). FABP shows increased plasma concentrations within 3 h after AMI and returns to a normal reference interval within 12–24 h, thereby resembling myoglobin (4)(5). However, the diagnostic specificity and sensitivity of FABP for AMI detection are better than those of myoglobin (6)(7). FABP is also found in skeletal muscle, but the determination of the plasma ratio of myoglobin over FABP allows the discrimination between myocardial and skeletal muscle injury (4)(5).

The application of FABP as an early plasma marker in routine clinical practice requires the availability of a rapid assay system. Several immunochemical assays for FABP have been described, taking an assay time of 2–16 h (2)(3)(8)(9). Recently, a one-step ELISA for plasma FABP with a total performance time of 45 min (10) and an amperometric enzyme immunosensor assay taking 27 min per plasma sample were described (11). However, these assays are of limited use for routine clinical practice. We describe here a microparticle-enhanced turbidimetric immunoassay for FABP that offers the advantages of being precise, easy to perform, rapid, and fully automated.

Latex reagent was prepared by physical adsorption onto carboxylated latex particles of three monoclonal anti-human FABP antibodies that recognize distinct epitopes (12), which were then stored in 10 mmol/L Tris-HCL, pH 8.0, containing 5 g/L bovine serum albumin, 0.01 g/L Tween 20, 1 g/L NaN3, and 50 g/L sucrose. The assay was performed by using a COBAS® MIRA Plus analyzer (F. Hoffmann-La Roche Ltd.). Briefly, 75 μL of latex reagent was mixed with 155 μL of reaction buffer (22 mmol/L phosphate buffer, pH 7.0, 350 mmol/L NaCl, 2 …

Development of a rapid microparticle-enhanced turbidimetric immunoassay for plasma fatty acid-binding protein, an early marker of acute myocardial infarction.

Jan F. C. Glatz

Papers

Molecular cloning of fatty acid-transport protein cDNA from rat.

Fatty acid transport proteins facilitate fatty acid uptake in skeletal muscle.

Lipids and lipid binding proteins: a perfect match.

Enzyme immunosensor for diagnosis of myocardial infarction

Development of a rapid microparticle-enhanced turbidimetric immunoassay for plasma fatty acid-binding protein, an early marker of acute myocardial infarction.