Effect of Window and Hole Pattern Cut-Outs on Design Optimization of 3D Printed Braces.

Background: There are many different Thoracic Lumbar Sacral Orthosis style brace designs available in the market for the correction of scoliosis deformity. Hole cut out patterns, are commonly used in brace designs. These cut-outs may be subdivided into two groups: hole patterns and windows.

The relationship between insulin and glucagon concentrations in non-diabetic humans.

Abnormal postprandial suppression of glucagon in Type 2 diabetes (T2DM) has been attributed to impaired insulin secretion. Prior work suggests that insulin and glucagon show an inverse coordinated relationship. However, dysregulation of α-cell function in prediabetes occurs early and independently of changes in β-cells, which suggests insulin having a less significant role on glucagon control.

Chromogranin A-positive hormone-negative endocrine cells in pancreas in human pregnancy.

Introduction: We sought to determine whether chromogranin A-positive hormone-negative (CPHN) endocrine cells are increased in the pancreas of pregnant women, offering potential evidence in support of neogenesis.

Methods: Autopsy pancreata from pregnant women ( = 14) and age-matched non-pregnant control women ( = 9) were obtained. Staining of pancreatic sections for chromogranin A, insulin and a cocktail of glucagon, somatostatin, pancreatic polypeptide and ghrelin was undertaken, with subsequent evaluation for CPHN cell frequency.

Insulin Pulse Characteristics and Insulin Action in Non-diabetic Humans.

Objective: Pulsatile insulin secretion is impaired in diseases such as type 2 diabetes that are characterized by insulin resistance. This has led to the suggestion that changes in insulin pulsatility directly impair insulin signaling. We sought to examine the effects of pulse characteristics on insulin action in humans, hypothesizing that a decrease in pulse amplitude or frequency is associated with impaired hepatic insulin action.

Diabetes-associated genetic variation in TCF7L2 alters pulsatile insulin secretion in humans.

BACKGROUNDMetabolic disorders such as type 2 diabetes have been associated with a decrease in insulin pulse frequency and amplitude. We hypothesized that the T allele at rs7903146 in TCF7L2, previously associated with β cell dysfunction, would be associated with changes in these insulin pulse characteristics.METHODSTwenty-nine nondiabetic subjects (age 46 ± 2, BMI 28 ± 1 kg/m2) participated in this study.

Fasting glucagon concentrations are associated with longitudinal decline of β-cell function in non-diabetic humans.

Purpose: Abnormal glucagon concentrations are a feature of prediabetes but it is uncertain if α-cell dysfunction contributes to a longitudinal decline in β-cell function. We therefore sought to determine if a decline in β-cell function is associated with a higher nadir glucagon in the postprandial period or with higher fasting glucagon.

Methods: This was a longitudinal study in which 73 non-diabetic subjects were studied on 2 occasions 6.

Identification of osteoclast-osteoblast coupling factors in humans reveals links between bone and energy metabolism.

Bone remodeling consists of resorption by osteoclasts followed by formation by osteoblasts, and osteoclasts are a source of bone formation-stimulating factors. Here we utilize osteoclast ablation by denosumab (DMAb) and RNA-sequencing of bone biopsies from postmenopausal women to identify osteoclast-secreted factors suppressed by DMAb. Based on these analyses, LIF, CREG2, CST3, CCBE1, and DPP4 are likely osteoclast-derived coupling factors in humans.

Pancreatic alpha-cell mass across adult human lifespan.

Aim: To establish pancreatic alpha-cell mass in lean, non-diabetic humans over the adult lifespan, performed as a follow-up study to beta-cell mass across the adult human lifespan.

Methods: We examined human pancreatic autopsy tissue from 66 lean, non-diabetic individuals aged from 30 to 102 years, grouped into deciles: 3rd (30-39 years), 4th (40-49 years), 5th (50-59 years), 6th (60-69 years), 7th (70-79 years), 8th (80-89 years) and 9th deciles (90+ years). Sections of pancreas were immunostained for glucagon and analyzed for fractional alpha-cell area.

Assessment of pulsatile insulin secretion derived from peripheral plasma C-peptide concentrations by nonparametric stochastic deconvolution.

The characteristics of pulsatile insulin secretion are important determinants of type 2 diabetes pathophysiology, but they are understudied due to the difficulties in measuring pulsatile insulin secretion noninvasively. Deconvolution of either peripheral C-peptide or insulin concentrations offers an appealing alternative to hepatic vein catheterization. However, to do so, there are a series of methodological challenges to overcome.

Characterization of Non-hormone Expressing Endocrine Cells in Fetal and Infant Human Pancreas.

Previously, we identified chromograninA positive hormone-negative (CPHN) cells in high frequency in human fetal and neonatal pancreas, likely representing nascent endocrine precursor cells. Here, we characterize the putative endocrine fate and replicative status of these newly formed cells. To establish the replicative frequency and transcriptional identity of CPHN cells, extending our observation on CPHN cell frequency to a larger cohort of fetal and infant pancreas.

Increased Rates of Meal Absorption Do Not Explain Elevated 1-Hour Glucose in Subjects With Normal Glucose Tolerance.

Context: In subjects with normal fasting glucose (NFG) and normal glucose tolerance (NGT), glucose concentrations >155 mg/dL 1 hour after 75 g of oral glucose predict increased risk of progression to diabetes. Recently, it has been suggested that the mechanism underlying this abnormality is increased gut absorption of glucose.

Objective: We sought to determine the rate of systemic appearance of meal-derived glucose in subjects classified by their 1-hour glucose after a 75-g oral glucose challenge.

Contribution of endogenous glucagon-like peptide-1 to changes in glucose metabolism and islet function in people with type 2 diabetes four weeks after Roux-en-Y gastric bypass (RYGB).

Unlabelled: Glucagon-Like Peptide-1 (GLP-1) is an insulin secretagogue which is elevated after Roux-en-Y Gastric Bypass (RYGB). However, its contribution to glucose metabolism after RYGB remains uncertain.

Aims: We tested the hypothesis that GLP-1 lowers postprandial glucose concentrations and improves β-cell function after RYGB.

An Increase in Chromogranin A-Positive, Hormone-Negative Endocrine Cells in Pancreas in Cystic Fibrosis.

We sought to establish whether an increase in chromogranin A-positive, hormone-negative (CPHN) endocrine cells occurs in the pancreas of patients with cystic fibrosis (CF), as potential evidence of neogenesis. Pancreata were obtained at autopsy from nondiabetic patients with CF (n = 12) and age-matched nondiabetic control subject (CS) individuals without CF (n = 12). In addition, pancreas from three diabetic patients with CF was obtained.

Effect of an elongation bending derotation brace on the infantile or juvenile scoliosis.

Background: A wide variety of braces are commercially available designed for the adolescent idiopathic scoliosis (AIS), but very few braces for infantile scoliosis (IS) or juvenile scoliosis (JS). The goals of this study were: 1) to briefly introduce an elongation bending derotation brace (EBDB) in the treatment of IS or JS; 2) to investigate changes of Cobb angles in the AP view of X-ray between in and out of the EBDB at 0, 3, 6, 9, and 12 months; 3) to compare differences of Cobb angles (out of brace) in 3, 6, 9, and12 month with the baseline; 4) to investigate changes (out of brace) in JS and IS groups separately.

Methods: Thirty-eight patients with IS or JS were recruited retrospectively for this study.

Paradigm Shifts in Nocturnal Glucose Control in Type 2 Diabetes.

Context: A better understanding of nocturnal regulation of glucose homeostasis will provide the framework for designing rational therapeutic strategies to improve the management of overnight glucose in patients with type 2 diabetes (T2D).

Objective: To establish the nocturnal pattern and regulation of glucose production (EGP) in humans and to determine whether the pattern is dysregulated in people with T2D.

Design: Subjects were infused with [3-3H] glucose overnight.

Increased Chromogranin A-Positive Hormone-Negative Cells in Chronic Pancreatitis.

Context: Chronic pancreatitis (CP) is characterized by inflammation, fibrosis, and a loss of pancreatic acinar cells, which can result in exocrine and eventually endocrine deficiency. Pancreatitis has been reported to induce formation of new endocrine cells (neogenesis) in mice. Our recent data have implicated chromogranin A-positive hormone-negative (CPHN) cells as potential evidence of neogenesis in humans.

Fixation Strength of Polyetheretherketone Sheath-and-Bullet Device for Soft Tissue Repair in the Foot and Ankle.

Tendon transfers are often performed in the foot and ankle. Recently, interference screws have been a popular choice owing to their ease of use and fixation strength. Considering the benefits, one disadvantage of such devices is laceration of the soft tissues by the implant threads during placement that potentially weaken the structural integrity of the grafts.

Impaired Insulin Action Is Associated With Increased Glucagon Concentrations in Nondiabetic Humans.

Context: Abnormal glucagon concentrations contribute to hyperglycemia, but the mechanisms of α-cell dysfunction in prediabetes are unclear.

Objective: We sought to determine the relative contributions of insulin secretion and action to α-cell dysfunction in nondiabetic participants across the spectrum of glucose tolerance.

Design: This was a cross-sectional study.

Performance of individually measured vs population-based C-peptide kinetics to assess β-cell function in the presence and absence of acute insulin resistance.

Aims: To compare the performance of population-based kinetics with that of directly measured C-peptide kinetics when used to calculate β-cell responsivity indices, and to study people with and without acute insulin resistance to ensure that population-based kinetics apply to all conditions where β-cell function is measured.

Methods: Somatostatin was used to inhibit endogenous insulin secretion in 56 people without diabetes. Subsequently, a C-peptide bolus was administered and the changing concentrations were used to calculate individual kinetic measures of C-peptide clearance.

Down Syndrome-Associated Diabetes Is Not Due To a Congenital Deficiency in Cells.

Aims/hypothesis: We sought to establish whether the increased incidence of diabetes associated with Down syndrome was due to a congenital deficit in cells.

Methods: The pancreas was obtained at autopsy from nondiabetic subjects with Down syndrome (n = 29) and age-matched nondiabetic control subjects without Down syndrome (n = 28). The pancreas sections were evaluated for the fractional -cell area.

Glucose metabolism during rotational shift-work in healthcare workers.

Aims/hypothesis: Shift-work is associated with circadian rhythm disruption and an increased risk of obesity and type 2 diabetes. We sought to determine the effect of rotational shift-work on glucose metabolism in humans.

Methods: We studied 12 otherwise healthy nurses performing rotational shift-work using a randomised crossover study design.

Mechanisms Underlying the Pathogenesis of Isolated Impaired Glucose Tolerance in Humans.

Context: Prediabetes is a heterogeneous disorder classified on the basis of fasting glucose concentrations and 2-hour glucose tolerance.

Objective: We sought to determine the relative contributions of insulin secretion and action to the pathogenesis of isolated impaired glucose tolerance (IGT).

Design: The study consisted of an oral glucose tolerance test and a euglycemic clamp performed in two cohorts matched for anthropometric characteristics and fasting glucose but discordant for glucose tolerance.

Increased Frequency of Hormone Negative and Polyhormonal Endocrine Cells in Lean Individuals With Type 2 Diabetes.

Context: It has been suggested that beta cell loss in type 2 diabetes (T2D) may be due to beta cell degranulation and/or altered cell identity. While shown to have a minor role in obese T2D, this has not been evaluated in lean T2D.

Objective: To establish the contribution of altered beta cell identity in lean T2D and, using a rodent model of lean T2D, whether changes in beta cell identity precede hyperglycemia.