Cardiomodulatory Effects of Cardiometabolic and Antihyperglycemic Medications: The Roles of Oxidative and Endoplasmic Reticulum Stress.

Uncontrolled hyperglycemia in people with diabetes is an established risk of premature cardiovascular disease. Repeated hypoglycemic events are also associated with increased cardiovascular mortality. Both hyperglycemia and hypoglycemia induce cellular stress, notably endoplasmic reticulum (ER) stress, a known promoter of cardiovascular disease.

Cross-section of thyroidology and nephrology: Literature review and key points for clinicians.

There are several key points clinicians should consider when managing patients with overlapping thyroid and renal disease. Patients who are euthyroid and have chronic kidney disease (CKD) may physiologically have normal-high thyroid stimulating hormone (TSH), low free thyroxine (FT4), low free triiodothyronine (FT3) and normal-low reverse triiodothyronine (rT3). Untreated subclinical and primary hypothyroidism among patients with (CKD) is associated with reversible progression of renal failure.

Cardioprotective antihyperglycemic drugs ameliorate endoplasmic reticulum stress.

Cellular stress, notably oxidative, inflammatory, and endoplasmic reticulum (ER) stress, is implicated in the pathogenesis of cardiovascular disease. Modifiable risk factors for cardiovascular disease such as diabetes, hypercholesterolemia, saturated fat consumption, hypertension, and cigarette smoking cause ER stress whereas currently known cardioprotective drugs with diverse pharmacodynamics share a common pleiotropic effect of reducing ER stress. Selective targeting of oxidative stress with known antioxidative vitamins has been ineffective in reducing cardiovascular risk.

Diabetes-related perturbations in the integrity of physiologic barriers.

One of the hallmarks of health is the integrity of barriers at the cellular and tissue levels. The two cardinal functions of barriers include preventing access of deleterious elements of the environment (barrier function) while facilitating the transport of essential ions, signaling molecules and nutrients needed to maintain the internal milieu (transport function). There are several cellular and subcellular barriers and some of these barriers can be interrelated.

Proton Therapy for Bilateral Breast Cancer Maximizes Normal-Tissue Sparing.

Purpose: Treatment for bilateral breast cancer with radiation therapy is technically challenging. We evaluated the clinical and dosimetric outcomes of a small series of patients with synchronous bilateral breast cancer, including a photon dosimetric comparison, to identify optimal treatment planning approaches.

Materials And Methods: We reviewed a registry of patients (simultaneously) diagnosed with synchronous bilateral breast cancers who underwent postoperative definitive adjuvant proton therapy at our institution between 2012 and 2021.

Management of Intraoperative Contamination of the Custom Total Temporomandibular Joint Prosthesis.

Management of intraoperative contamination of a custom total temporomandibular joint prosthesis has not been reported in the literature. As this complication is rare, it can be unsettling for the surgeon. Improper management may lead to a complicated treatment course and financial consequences.

Transcription factor EB protects against endoplasmic reticulum stress in human coronary artery endothelial cells.

Oxidative stress and endoplasmic reticulum (ER) stress promote atherogenesis while transcription factor EB (TFEB) inhibits atherosclerosis. Since reducing oxidative stress with antioxidants have failed to reduce atherosclerosis possibly because of aggravation of ER stress, we studied the effect of TFEB on ER stress in human coronary artery endothelial cells. ER stress was measured using the secreted alkaline phosphatase assay.

Differential effects of cyclooxygenase-2 (COX-2) inhibitors on endoplasmic reticulum (ER) stress in human coronary artery endothelial cells.

Selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib was pulled off the market because of its association with increased risk of adverse cardiovascular effects. The precise underlying mechanism for the differential effects of COX-2 inhibitors on cardiovascular risk is not known. Since endoplasmic reticulum (ER) stress is implicated in atherogenesis, we examined the effects of COX-2 inhibitors on ER stress in primary human coronary artery endothelial cells (HCAEC), human umbilical vein endothelial cells (HUVEC), and human pulmonary artery endothelial cells (HPAEC).

Characteristics of Serrated Adenomas in Non-Hispanic Whites and African Americans Undergoing Screening Colonoscopy.

Background and aim Adenomatous polyps are precursor lesions for colorectal cancer (CRC). Serrated adenomas/polyps are considered a risk factor for the development of proximal and interval CRC. African-Americans are at higher risk for right-sided CRC.

Effect of anti-hyperglycemic drugs on endoplasmic reticulum (ER) stress in human coronary artery endothelial cells.

Endoplasmic reticulum (ER) stress plays a critical role in progression of diabetes and development of complications, notably cardiovascular disease. Some of the contemporary anti-hyperglycemic drugs have been shown to inhibit ER stress. To extend these observations, the effects of various anti-hyperglycemic agents were screened for their effects on ER stress.

Bedside ultrasound-guided aspiration and corticosteroid injection of a baker's cyst in a patient with osteoarthritis and recurrent knee pain.

Baker's cyst accompanying knee osteoarthritis represents a common cause of knee pain presenting to the emergency department. In this case report, a 56-year-old male presented with atraumatic left knee pain and swelling. Radiographically, he had tricompartmental osteoarthritis and was found to have a baker's cyst on duplex ultrasound.

The effect of nicotine and dextrose on endoplasmic reticulum stress in human coronary artery endothelial cells.

Cigarette smoking is one of the major causes of coronary artery disease (CAD) as is diabetes. However, nicotine has been generally regarded as safe and is used in smoking cessation programs. This presumption of nicotine safety was examined in human coronary artery endothelial cells (HCAEC).

Reduced cellular glucose transport confers natural protection against dextrose-induced superoxide generation and endoplasmic reticulum stress in domestic hen.

Normal blood glucose levels in avian species are two to fourfold higher than that in humans and the higher blood glucose levels in birds do not cause adverse effects. Endothelial cells isolated from the aorta of the domestic hen (Gallus gallus domesticus) and chicken aortic smooth muscle cells (CAOSMC) were compared to human coronary artery endothelial cells (HCAEC) and human primary aortic smooth muscle cells (HASMC). Superoxide (SO) generation was measured using a superoxide-reactive probe.

Triceps Tendon Injuries.

Triceps tendon injuries are an uncommon clinical entity poorly described in the literature. This review discusses the spectrum of pathology, effective diagnosis, nonsurgical treatment, surgical treatment, rehabilitation, and surgical complications of triceps tendon injuries. Management of triceps tendinopathies depends on the mechanism of injury and the patient's motor examination.

High-throughput analysis identifying drugs that reduce oxidative and ER stress in human coronary artery endothelial cells.

Endoplasmic reticulum (ER) stress as well as oxidative stress have been shown to play important roles in metabolic and cardiovascular disease, and drugs that counteract the effects of ER and oxidative stresses may be clinically useful. To identify novel compounds that ameliorate ER and oxidative stresses, we screened two drug libraries purchased from Evotec, San Francisco, CA; the NIH clinical collection 1 (446 compounds) and the NIH clinical collection 2 (281 compounds). Human coronary artery endothelial cells (HCAEC) were tested for ER and oxidative stress.

Inhibition of Pro-Inflammatory Cytokine Secretion by Select Antioxidants in Human Coronary Artery Endothelial Cells.

Inflammatory and oxidative stress in endothelial cells are implicated in the pathogenesis of premature atherosclerosis in diabetes. To determine whether high-dextrose concentrations induce the expression of pro-inflammatory cytokines, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 or 27.

Regulation of apolipoprotein A-I gene expression by the histamine H1 receptor: Requirement for NF-κB.

Aims: Earlier it had been found by us that apolipoprotein A-I (apo A-I) is suppressed by histamine in HepG2 cells. Histamine has been shown to regulate NF-κB activity, though not in hepatocytes. Therefore we examined the role of the histamine receptors and NF-κB in histamine-mediated apo A-I gene expression in HepG2 liver cells.

Inhibition of hepatic apolipoprotein A-I gene expression by histamine.

In a recent high throughput analysis to identify drugs that alter hepatic apolipoprotein A-I (apo A-I) expression, histamine receptor one (H) antagonists emerged as potential apo A-1 inducing drugs. Thus the present study was undertaken to identify some of the underlying molecular mechanisms of the effect of antihistaminic drugs on apo AI production. Apo A-I levels were measured by enzyme immunoassay and Western blots.

Immediate Reconstruction and Dental Rehabilitation of Segmental Mandibular Defects: Description of a Novel Technique.

The aim of this report is to present a new technique using current technologic advances for immediate reconstruction and dental rehabilitation of segmental mandibular defects with a screw-retained prosthesis. One case is reviewed and a detailed review of surgical and prosthetic techniques used is presented.

Pro-inflammatory signaling by 24,25-dihydroxyvitamin D3 in HepG2 cells.

The vitamin D metabolite 24,25-dihydroxyvitamin D3 (24, 25[OH]2D3) was shown to induce nongenomic signaling pathways in resting zone chondrocytes and other cells involved in bone remodeling. Recently, our laboratory demonstrated that 24,25-[OH]2D3 but not 25-hydroxyvitamin D3, suppresses apolipoprotein A-I (apo A-I) gene expression and high-density lipoprotein (HDL) secretion in hepatocytes. Since 24,25-[OH]2D3 has low affinity for the vitamin D receptor (VDR) and little is known with regard to how 24,25-[OH]2D3 modulates nongenomic signaling in hepatocytes, we investigated the capacity of 24,25-[OH]2D3 to activate various signaling pathways relevant to apo A-I synthesis in HepG2 cells.

Induction of apolipoprotein A-I gene expression by glucagon-like peptide-1 and exendin-4 in hepatocytes but not intestinal cells.

Objective: Diabetic dyslipidemia is an important risk factor for the development of macrovascular complications. Recent clinical trials suggest that diabetics treated with glucagon-like peptide-1 (GLP-1) have normalized lipid levels, including an increase in plasma high-density lipoprotein cholesterol (HDLc) levels.

Methods: To determine if GLP-1 (7-36 amide) and the GLP-1-like insulinotropic peptide exendin-4 regulate expression of apolipoprotein A-I (apo A-I), the primary anti-atherogenic component of high-density lipoprotein (HDL), HepG2 hepatocytes and Caco-2 intestinal cells, representative of tissues that express the majority of apo A-I, were treated with increasing amounts of each peptide and apo A-I gene expression was measured in the conditioned medium.

The emerging evidence for vitamin D-mediated regulation of apolipoprotein A-I synthesis.

Ischemic heart disease and cerebrovascular ischemia are leading causes of mortality in industrialized countries. The pathogenesis of these diseases involves the formation of atherosclerotic plaques with eventual rupture and superimposed thrombosis. This process is inhibited by high-density lipoprotein (HDL), the main protein component of which is apolipoprotein A-I (apo A-I).

Inflammation, high-density lipoprotein and cardiovascular dysfunction.

Purpose Of Review: This review describes the evidence that supports the hypothesis that high-density lipoprotein (HDL) is atheroprotective due to its antiinflammatory effects and benefits on vascular health.

Recent Findings: Recent investigations have shown that HDL may inhibit atherosclerosis by promoting healthy endothelial function and by limiting or inhibiting the activation of macrophage and other immune cells. Receptors for HDL clearly regulate immune system function as well as cellular stress.