To focus attention of the clinician on the anatomy and (patho)physiology of the vertebral venous system, so as to offer a tool to better understand and anticipate (potential) complications that are related to the application of percutaneous vertebroplasty and kyphoplasty. Percutaneous vertebroplasty and kyphoplasty are newly developed, minimally invasive techniques for the relief of pain and for the strengthening of bone in vertebral body lesions. With the clinical implementation of these techniques, a number of serious neurologic and cardiopulmonary complications have been reported in the international medical literature. Most complications appear to be related to the extrusion of bone cement into the vertebral venous system. The literature about complications of percutaneous vertebroplasty and kyphoplasty is reviewed, and the anatomic and (patho)physiologic characteristics of the vertebral venous system are reported. Based on what is currently known from the anatomy and physiology of the vertebral venous system, the procedures of percutaneous vertebroplasty and kyphoplasty are analyzed, and suggestions are made to improve the safety of these techniques. Thorough knowledge of the anatomic and (patho)physiologic characteristics of the vertebral venous system is mandatory for all physicians that participate in percutaneous vertebroplasty and kyphoplasty. To reduce the risk of cement extrusion into the vertebral venous system during injection, vertebral venous pressure should be increased during surgery. This can be achieved by operating the patient in the prone position and by raising intrathoracic venous pressure with the aid of the anesthesiologist during intravertebral instrumentation and cement injection. Intensive theoretical and practical training, critical patient selection, and careful monitoring of the procedures, also taking into account patient positioning and intrathoracic and intra-abdominal pressures, will help to facilitate low morbidity outcomes inthese very promising minimally invasive techniques.

Diabetic patients are at an increased risk of developing heart failure when compared to their non-diabetic counter parts. Accumulative evidence suggests chronic hyperglycemia to be central in the development of myocardial infarction in these patients. At present, there are limited therapies aimed at specifically protecting the diabetic heart at risk from hyperglycemia-induced injury. Oxidative stress, through over production of free radical species, has been hypothesized to alter mitochondrial function and abnormally augment the activity of the NADPH oxidase enzyme system resulting in accelerated myocardial injury within a diabetic state. This has led to a dramatic increase in the exploration of plant-derived materials known to possess antioxidative properties. Several edible plants contain various natural constituents, including polyphenols that may counteract oxidative-induced tissue damage through their modulatory effects of intracellular signaling pathways. Rooibos, an indigenous South African plant, well-known for its use as herbal tea, is increasingly studied for its metabolic benefits. Prospective studies linking diet rich in polyphenols from rooibos to reduced diabetes associated cardiovascular complications have not been extensively assessed. Aspalathin, a flavonoid, and phenylpyruvic acid-2-O-β-D-glucoside, a phenolic precursor, are some of the major compounds found in rooibos that can ameliorate hyperglycemia-induced cardiomyocyte damage in vitro. While the latter has demonstrated potential to protect against cell apoptosis, the proposed mechanism of action of aspalathin is linked to its capacity to enhance the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression, an intracellular antioxidant response element. Thus, here we review literature on the potential cardioprotective properties of flavonoids and a phenylpropenoic acid found in rooibos against diabetes-induced oxidative injury.

Although pancreatic β-cells are capable of adapting their mass in response to insulin requirements, evidence has shown that a dietary insult could compromise this ability. Fetal malnutrition has been linked to low birth weight and the development of type 2 diabetes later in life, while reduced β-cell mass has been reported in adult rats fed a high-fat diet (HFD). Reported here are the effects of exposure to a HFD, during different periods of gestation, on neonatal rat weight and β- and α-cell development. The experimental groups were composed of neonatal offspring obtained from Wistar rats fed a high-fat (40% as energy) diet for either the first (HF1), second (HF2), or third (HF3) week, or all three (HF1–3) weeks of gestation. Neonatal weights and circulating glucose and insulin concentrations were measured on postnatal day 1, after which the pancreata were excised and processed for histological immunocytochemical examination and image analysis. HF1 and HF2 neonates were hypoglycemic, whereas HF1–3 neonates were hyperglycemic. Low birth weights were observed only in HF1 neonates. No significant differences were detected in the circulating insulin concentrations in the neonates, although β-cell volume and numbers were reduced in HF1–3 neonates. β-cell numbers also declined in HF1 and HF3 neonates. α-cell volume, number and size were, however, increased in HF1–3 neonates. α-cell size was also increased in HF1 and HF3 neonates. In neonates, exposure to a maternal HFD throughout gestation was found to have the most adverse effect on β-cell development and resulted in hyperglycemia.