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1.
Obes Surg ; 31(3): 1004-1012, 2021 03.
Article in English | MEDLINE | ID: mdl-32827094

ABSTRACT

OBJECTIVE: Bariatric surgery presents a long-term solution for clinical obesity. Given that Black Americans (BA) carry a greater burden of obesity-related comorbidities than White Americans (WA), understanding the racial disparities regarding remission of obesity comorbidities following the most common bariatric surgery, sleeve gastrectomy (SG). The goal of the current study was to provide quantitative values related to cardiovascular and lipid outcomes following SG and determine if racial disparities exist between BA and WA. METHODS: Data was collected from de-identified electronic medical records for patients receiving SG surgery at the University of Mississippi Medical Center in Jackson, MS, USA. RESULTS: Of 464 patients who obtained SG from (2013-2019), 64% were WA, and 36% were BA. Before surgery, BA had significantly greater body weight (BW), body mass index (BMI), and systolic (SBP) and diastolic (DBP) blood pressures (BP) in comparison with WA. Compared with WA, BA were predicted to lose 5.1 kg less BW than WA at 1-year follow-up. Reduction in SBP (- 0.96 vs. - 0.60 mmHg/doubling of days) and DBP (- 0.51 vs. - 0.26 mmHg/doubling of days) was significantly higher in WA compared with BA. There was no racial difference in the change to total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, or triglycerides by race. When normalized to weight loss, the racial disparity in BP reduction was mitigated. CONCLUSIONS: These data indicate that BA lose less body weight following SG; however, loss of excess body weight loss is associated with improvement to BP similarly in both BA and WA.


Subject(s)
Cardiovascular Diseases , Obesity, Morbid , Black or African American , Gastrectomy , Heart Disease Risk Factors , Humans , Obesity, Morbid/surgery , Risk Factors
3.
Physiol Rep ; 2(2): e00231, 2014 Feb 01.
Article in English | MEDLINE | ID: mdl-24744900

ABSTRACT

The acute response of parathyroid hormone to perturbations in serum ionized calcium ([Ca(2+)]) is physiologically complex, and poorly understood. The literature provides numerous observations of quantitative and qualitative descriptions of parathyroid hormone (PTH) dynamics. We present a physiologically based mathematical model of PTH secretion constructed from mechanisms suggested in the literature, and validated against complex [Ca(2+)] clamping protocols from human data. The model is based on two assumptions. The first is that secretion is a fraction of cellular reserves, with the fraction being determined by the kinetics of [Ca(2+)] with its receptor. The second is that there are multiple distinct populations of parathyroid cells, with different secretory parameters. The steady state and transient PTH secretion responses of the model are in agreement with human experimental PTH responses to different hypocalcemia and hypercalcemia stimuli. This mathematical model suggests that a population of secreting cells is responsible for the PTH secretory dynamics observed experimentally.

4.
PLoS One ; 8(9): e74329, 2013.
Article in English | MEDLINE | ID: mdl-24058546

ABSTRACT

We present a small integrative model of human cardiovascular physiology. The model is population-based; rather than using best fit parameter values, we used a variant of the Metropolis algorithm to produce distributions for the parameters most associated with model sensitivity. The population is built by sampling from these distributions to create the model coefficients. The resulting models were then subjected to a hemorrhage. The population was separated into those that lost less than 15 mmHg arterial pressure (compensators), and those that lost more (decompensators). The populations were parametrically analyzed to determine baseline conditions correlating with compensation and decompensation. Analysis included single variable correlation, graphical time series analysis, and support vector machine (SVM) classification. Most variables were seen to correlate with propensity for circulatory collapse, but not sufficiently to effect reasonable classification by any single variable. Time series analysis indicated a single significant measure, the stressed blood volume, as predicting collapse in situ, but measurement of this quantity is clinically impossible. SVM uncovered a collection of variables and parameters that, when taken together, provided useful rubrics for classification. Due to the probabilistic origins of the method, multiple classifications were attempted, resulting in an average of 3.5 variables necessary to construct classification. The most common variables used were systemic compliance, baseline baroreceptor signal strength and total peripheral resistance, providing predictive ability exceeding 90%. The methods presented are suitable for use in any deterministic mathematical model.


Subject(s)
Cardiovascular Physiological Phenomena , Models, Cardiovascular , Baroreflex/physiology , Blood Pressure , Blood Volume , Calibration , Carbon Monoxide/metabolism , Heart Failure/physiopathology , Hemorrhage/physiopathology , Homeostasis , Humans , Pressoreceptors/metabolism , Support Vector Machine , Survival Analysis , Time Factors , Vascular Resistance
5.
J Theor Biol ; 296: 1-5, 2012 Mar 07.
Article in English | MEDLINE | ID: mdl-22154846

ABSTRACT

It has been noted in multiple studies that the calcium-PTH axis, among others, is subject to an apparent hysteresis. We sought to explain a major component of the observed phenomenon by constructing a simple mathematical model of a hormone and secretagogue system with concentration dependent secretion and containing two delays. We constructed profiles of the hormone-agonist axis in this model via four types of protocols, three of which emulating experiments from the literature, and observed a delay- and load-dependent hysteresis that is an expected mathematical artifact of the system described. In particular, the delay associated with correction allows for over-secretion of the hormone influencing the corrective mechanism; thus rate dependence is an artifact of the corrective mechanism, not a sensitivity of the gland to the magnitude of change. From these observations, the detected hysteresis is due to delays inherent in the systems being studied, not in the secretory mechanism.


Subject(s)
Calcium/physiology , Models, Biological , Parathyroid Hormone/metabolism , Calcium/blood , Homeostasis/physiology , Humans , Parathyroid Hormone/agonists , Parathyroid Hormone/blood
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