Obesity is a heterogeneous disorder. Obese individuals vary in their body fat distribution, their metabolic profile and degree of associated cardiovascular and metabolic risk. Abdominal obesity carries greater risk of developing diabetes and future cardiovascular events than peripheral or gluteofemoral obesity. There are differences between adipose tissue present in subcutaneous areas (SCAT) and visceral adipose tissue (VAT) present in the abdominal cavity. These include anatomical, cellular, molecular, physiological, clinical and prognostic differences. Anatomically, VAT is present mainly in the mesentery and omentum, and drains directly through the portal circulaion to the liver. VAT compared with SCAT is more cellular, vascular, innervated and contains a larger number of inflammatory and immune cells, lesser preadipocyte differentiating capacity and a greater percentage of large adipocytes. There are more glucocorticoid and androgen receptors in VAT than in SCAT. VAT adipocytes are more metabolically active, more sensitive to lipolysis and more insulin-resistant than SCAT adipocytes. VAT has a greater capacity to generate free fatty acids and to uptake glucose than SCAT and is more sensitive to adrenergic stimulation, while SCAT is more avid in absorption of circulating free fatty acids and triglycerides. VAT carries a greater prediction of mortality than SCAT.

Kinins generated intrarenally probably affect renal function by altering levels of various mediators and messengers, including prostaglandin Ej (PGE 2 ) and cyclic guanosine 3',5'-monophosphate (cGMP). Using a microdialysis technique, we monitored levels of cortical and medullary renal interstitial fluid kinins, PGEz, and cGMP after 5 days of 0.15% (low), 0.28% (normal), or 4.0% (high) sodium intake. Samples were collected from anesthetized rats (n=5 for each diet). During normal sodium intake, renal interstitial fluid kinin, PGEj, and cGMP levels in dialysate leaving the cortex were 113+8 pg/min, 1.23±0.11 pg/min, and 0.05+0.004 pmol/min, respectively. In the fluid leaving the medulla, the levels were 93.0+17 pg/min, 2.28±0.14 pg/min, and 0.08±0.005 pmol/min, respectively. In rats consuming a low sodium diet, renal T here is much evidence to suggest that the endogenous renal kallikrein-kinin system is involved in the regulation of sodium and water excretion and arterial blood pressure.1 All the components of the system are present in the kidney, and their distribution is consistent with the probability of local actions within the kidney. "5 Kinins can stimulate production of both nitric oxide (NO) and eicosanoids. Bradykinin is known to release NO and prostacyclin from endothelial cells and isolated arterial preparations. 67 At least a portion of the renal effects of kinins are mediated by prostaglandins after a receptor interaction coupled to phospholipase A 2 .8 In addition, phospholipase C activation stimulates the formation of inositol 1,4,5-triphosphate, which triggers the release of calcium from intracellular storage sites. 9 The receptor-mediated translocation of intracellular calcium and influx of extracellular calcium can lead to the activation of NO synthase, which metabolizes L-arginine to NO in endothelial cells. NO can then stimulate cyclic 3',5'-guanosine monophosphate (cGMP) release from vascular smooth muscle cells.In the present study we evaluated the effects of sodium intake on the intrarenal levels of kinin, prostaglandin E 2 (PGE 2 ), and cGMP in the rat. We used a new renal interstitial fluid microdialysis technique (which has been used only in the dog) to sample rat renal cortical and medullary kinin, PGE?, and cGMP levels in response to low, normal, and high dietary sodium intakes.From the Departments of Internal Medicine and Pharmacology, University of Virginia Health Sciences Center (Charlottesville); Cairo University (Egypt); and Medical University of South Carolina (Charleston).Correspondence to Helmy M. Siragy, MD, Department of Medicine, Box 482, University of Virginia Health Sciences Center, Charlottesville, VA 22908. cortical interstitial fluid kinin and cortical and medullary PGEj and cGMP appearance rates were significantly increased (P<.01). Rats consuming a high sodium diet showed renal cortical and medullary kinin levels that were decreased 100-fold (/ J <.01), whereas PGE? and cGMP were increased (P<.01) compared with levels in rats with normal sodium intake. Renal...

Background Mobile health (mHealth) interventions are increasingly being designed to facilitate health-related behavior change. Integrating insights from behavioral science and design science can help support the development of more effective mHealth interventions. Behavioral Design (BD) and Design Thinking (DT) have emerged as best practice approaches in their respective fields. Until now, little work has been done to examine how BD and DT can be integrated throughout the mHealth design process. Objective The aim of this scoping review was to map the evidence on how insights from BD and DT can be integrated to guide the design of mHealth interventions. The following questions were addressed: (1) what are the main characteristics of studies that integrate BD and DT during the mHealth design process? (2) what theories, models, and frameworks do design teams use during the mHealth design process? (3) what methods do design teams use to integrate BD and DT during the mHealth design process? and (4) what are key design challenges, implementation considerations, and future directions for integrating BD and DT during mHealth design? Methods This review followed the Joanna Briggs Institute reviewer manual and PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews) checklist. Studies were identified from MEDLINE, PsycINFO, Embase, CINAHL, and JMIR by using search terms related to mHealth, BD, and DT. Included studies had to clearly describe their mHealth design process and how behavior change theories, models, frameworks, or techniques were incorporated. Two independent reviewers screened the studies for inclusion and completed the data extraction. A descriptive analysis was conducted. Results A total of 75 papers met the inclusion criteria. All studies were published between 2012 and 2021. Studies integrated BD and DT in notable ways, which can be referred to as “Behavioral Design Thinking.” Five steps were followed in Behavioral Design Thinking: (1) empathize with users and their behavior change needs, (2) define user and behavior change requirements, (3) ideate user-centered features and behavior change content, (4) prototype a user-centered solution that supports behavior change, and (5) test the solution against users’ needs and for its behavior change potential. The key challenges experienced during mHealth design included meaningfully engaging patient and public partners in the design process, translating evidence-based behavior change techniques into actual mHealth features, and planning for how to integrate the mHealth intervention into existing clinical systems. Conclusions Best practices from BD and DT can be integrated throughout the mHealth design process to ensure that mHealth interventions are purposefully developed to effectively engage users. Although this scoping review clarified how insights from BD and DT can be integrated during mHealth design, future research is needed to identify the most effective design approaches.

Objective-To investigate the functional significance of chronotropic incompetence during dobutamine stress echocardiography. Patients and methods-The functional significance of chronotropic incompetence was evaluated during dobutamine stress echocardiography in 512 patients without blocker treatment who underwent dobutamine stress echocardiography (up to 40 µg/kg/min) and completed the protocol or reached the target heart rate. Mean (SD) age was 60 (12) years (313 men, 199 women). Chronotropic incompetence was defined as failure to achieve 85% of the maximum exercise heart rate predicted for age and sex (220 − age in men; 200 − age in women) at maximum dobutamine dose. Results-Chronotropic incompetence occurred in 196 patients (38%). AVected patients were significantly younger, more likely to be men (both p << 0.001) and smokers (p < 0.05), had a higher prevalence of previous myocardial infarction (p < 0.005) and resting wall motion abnormalities (p < 0.05), and had a lower resting heart rate (p << 0.001) and systolic blood pressure (p << 0.001) than patients without chronotropic incompetence, but there was no diVerence in the overall prevalence of ischaemia and significant coronary artery disease. By multivariate analysis, independent predictors of chronotropic incompetence were a lower resting heart rate (p << 0.001), younger age (p << 0.001), and male sex (p << 0.001). Conclusions-The relations among sex, age, and chronotropic incompetence show the need to titrate the dobutamine dose using specific data based on age and sex related heart rate responses to dobutamine rather than to an exercise stress test. Obtaining specific heart rate criteria is necessary to determine whether chronotropic incompetence represents a real failure to achieve a normal response or is the result of applying an inappropriate gold standard. (Heart 1999;81:398-403)

The accuracy of ST segment elevation for the prediction of functional improvement was similar to that of low dose dobutamine echocardiography in patients with anterior infarction (80% v 83%) and in patients who underwent revascularisation (78% v 83% respectively). Conclusion-In patients with a recent Q wave myocardial infarction, dobutamineinduced ST segment elevation is a valuable marker of myocardial viability particularly when the test is performed without or with suboptimal echocardiographic imaging.